Strain Name:

B6.129S4-Ptentm1Hwu/J

Stock Number:

006440

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Availability:

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Use Restrictions Apply, see Terms of Use
When used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating neural tissue-specific mutants of the floxed allele. These mutant mice may be useful in studies of neurogenesis, glia differentiation, and cerebellar development, for example.

Description

Strain Information

Type Congenic; Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Mating SystemHomozygote x Homozygote         (Female x Male)   25-JAN-08
Specieslaboratory mouse
GenerationN11F7 (07-MAR-11)
Generation Definitions
 
Donating Investigator IMR Colony,   The Jackson Laboratory

Description
These mice possess loxP sites flanking exon 5 of the targeted gene. Mice homozygous for the "floxed" allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating tissue-specific mutants of the floxed allele.

For example, when crossed to a strain expressing Cre recombinase in astrocytes (see Stock No. 012887), this mutant mouse strain may be useful in studies of neurogenesis.

When crossed to a strain expressing Cre recombinase in the central nervous system (see Stock No. 004600), this mutant mouse strain may be useful in studies of glia differentiation and cerebellar development.

When crossed to B6.129X1-Twist2tm1.1(cre)Dor/J mice (Stock No. 008712) expressing Cre recombinase in mesoderm-derived tissues (including chondrocytes and osteoblasts) offspring die at birth and exhibit defects in angioblast differentiation.

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description as published results become available.

Development
A loxP site flanked targeting vector containing hygromycin resistance and thymidine kinase genes was used in the construction of this mutant. This selection cassette was inserted downstream of exon 5 of the targeted gene, and another loxP site was inserted upstream of exon 5. This construct was electroporated into 129S4/SvJae derived LW-1 embryonic stem (ES) cells, which were transiently transfected with a Cre-recombinase vector to remove the selection cassette. Correctly targeted ES cells were injected into BALB/c blastocysts. The resulting chimeric animals were crossed to BALB/cAnNTac mice before being made homozygous. The mice were then backcrossed onto the C57BL/6J background for at least 5 generations. Heterozygotes were then bred to generate homozygotes.

Control Information

  Control
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Ptentm1Hwu allele
013590   B6.Cg-Braftm1Mmcm Ptentm1Hwu Tg(Tyr-cre/ERT2)13Bos/BosJ
004597   C;129S4-Ptentm1Hwu/J
View Strains carrying   Ptentm1Hwu     (2 strains)

Additional Web Information

Introduction to Cre-lox technology

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).
Cowden Syndrome 1; CWS1
Thyroid Carcinoma, Follicular; FTC
- Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).
Alveolar Capillary Dysplasia with Misalignment of Pulmonary Veins;
Leukemia, Acute Lymphoblastic; ALL
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Bannayan-Riley-Ruvalcaba Syndrome; BRRS   (PTEN)
Endometrial Cancer   (PTEN)
Glioma Susceptibility 2; GLM2   (PTEN)
Macrocephaly/Autism Syndrome   (PTEN)
Melanoma, Cutaneous Malignant, Susceptibility to, 1; CMM1   (PTEN)
Meningioma, Familial, Susceptibility to   (PTEN)
Phosphatase and Tensin Homolog; PTEN   (PTEN)
Prostate Cancer   (PTEN)
Squamous Cell Carcinoma, Head and Neck; HNSCC   (PTEN)
Vacterl Association with Hydrocephalus   (PTEN)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain.

Ptentm1Hwu/Pten+

        involves: 129S4/SvJae * BALB/c
  • tumorigenesis
  • abnormal tumor incidence
    • spectrum of tumor incidence and onset on the BALB/c background are similar to Ptentm1.1Hwu on the BALB/c background in the first seven months   (MGI Ref ID J:110567)

Ptentm1Hwu/Ptentm1Hwu

        involves: 129S4/SvJae   (conditional)
  • tumorigenesis
  • increased prostate gland adenocarcinoma incidence
    • prostate adenocarcinoma is seen by 9-10 weeks of age in mutants infected with an adenovirus expressing Cre recombinase   (MGI Ref ID J:144810)
  • increased prostate intraepithelial neoplasia incidence
    • mutants infected with an adenovirus expressing Cre recombinase develop PIN by 7 weeks of age   (MGI Ref ID J:144810)
  • muscle phenotype
  • abnormal muscle fiber morphology
    • primary myotube cultures treated with adenovirus-cre to delete Pten results in increased myotube size   (MGI Ref ID J:169364)
    • primary myotube cultures treated with adenovirus-cre do not exhibit the palmitate-induced decrease in cell size seen in control myotubes   (MGI Ref ID J:169364)
  • homeostasis/metabolism phenotype
  • abnormal response to injury
    • mice injected neonatally with a cre-expressing adenovirus into the sensorimotor cortex and undergoing pyramidotomy in adulthood exhibit an increase in trans-midline sprouting of adult corticospinal tract axons compared to controls   (MGI Ref ID J:165283)
    • neonatal and postnatal deletion of Pten by injecting cre-expressing adenovirus into the sensorimotor cortex at the neonatal stage or 4 weeks of age, respectively, results in increased corticospinal tract regeneration following T8 complete spinal cord crush injury compared to controls   (MGI Ref ID J:165283)
    • the increase in corticospinal tract regeneration is seen when complete spinal cord crush is done at 2 and 5 months of age and the regenerating axons follow ectopic trajectories and extend bilaterally in contrast with normal unilateral extension in controls   (MGI Ref ID J:165283)
    • regenerating corticospinal tract axons after injury from mice injected with cre-expressing adenovirus are able to reform synaptic structures in the spinal cord caudal to the lesion site   (MGI Ref ID J:165283)

The following phenotype relates to a compound genotype created using this strain.
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Cd19tm1(cre)Cgn/Cd19+ Ptentm1Hwu/Ptentm1Hwu

        involves: 129P2/OlaHsd * 129S4/SvJae   (conditional)
  • hematopoietic system phenotype
  • abnormal B cell negative selection
    • bone marrow cultured with IL-7 over a 6 day period to promote selective expansion of pre-B cells exhibits an approximate 7-fold enhancement in the frequency of activated immature mutant B cells relative to immature wild-type B cells   (MGI Ref ID J:155314)
    • gating on activated B cells shows that immature mutant B cells proliferate to a much greater extent than immature wild-type B cells   (MGI Ref ID J:155314)
    • these experiments show that upon BCR engagement, immature B cells are activated and proliferate rather than being inhibited and undergoing anergy   (MGI Ref ID J:155314)
  • abnormal B cell physiology
    • B cells are responsive to chemotactic stimuli but show reduced directed movement toward the stimulus   (MGI Ref ID J:83213)
    • abnormal class switch recombination
      • impaired class-switch recombination in antibody secreting cells in response to a T-dependent antigen; B cells fail to undergo class-switch recombination to IgG3 or IgG1 in the presence of LPS or LPS plus IL-4, respectively   (MGI Ref ID J:114881)
      • however, well-formed germinal centers are observed in spleen after immunization   (MGI Ref ID J:114881)
    • decreased IgG level
      • decrease in IgG after TNP-OVA immunization   (MGI Ref ID J:114881)
    • increased B cell apoptosis
      • cultured B cells show increased apoptosis   (MGI Ref ID J:83213)
    • increased B cell proliferation
      • B cells are hyperproliferative in response to mitogenic stimuli and exhibit a lower threshold for activation through the B cell antigen receptor   (MGI Ref ID J:83213)
      • B cells exhibit altered cell cycle progression, with an increase in the percentage of cells in S and G2-M stages   (MGI Ref ID J:83213)
      • neonatal B cells proliferate strongly in response to both LPS and anti-IgM F(ab')2 unlike wild-type B cells which show a modest proliferation in response to LPS and no proliferation in response to the anti-IgM F(ab')2   (MGI Ref ID J:155314)
    • increased IgM level
      • increase in IgM after TNP-OVA immunization   (MGI Ref ID J:114881)
  • abnormal plasma cell morphology
    • increase in numbers of IgMhi antibody secreting cells and decrease in numbers of IgGhi antibody secreting cells   (MGI Ref ID J:114881)
  • decreased spleen germinal center number
    • reduction in germinal center formation in response to sheep red blood cell immunization and in response to environmental antigens   (MGI Ref ID J:83213)
  • increased B cell number
    • increase in the absolute number of splenic B cells, attributed mainly to the expansion/accumulation of MZ B cells   (MGI Ref ID J:83213)
    • increased B-1 B cell number
      • expansion of the B1 cell population   (MGI Ref ID J:83213)
    • increased marginal zone B cell number
      • expansion of the MZ B cell compartment   (MGI Ref ID J:83213)
  • immune system phenotype
  • abnormal B cell negative selection
    • bone marrow cultured with IL-7 over a 6 day period to promote selective expansion of pre-B cells exhibits an approximate 7-fold enhancement in the frequency of activated immature mutant B cells relative to immature wild-type B cells   (MGI Ref ID J:155314)
    • gating on activated B cells shows that immature mutant B cells proliferate to a much greater extent than immature wild-type B cells   (MGI Ref ID J:155314)
    • these experiments show that upon BCR engagement, immature B cells are activated and proliferate rather than being inhibited and undergoing anergy   (MGI Ref ID J:155314)
  • abnormal B cell physiology
    • B cells are responsive to chemotactic stimuli but show reduced directed movement toward the stimulus   (MGI Ref ID J:83213)
    • abnormal class switch recombination
      • impaired class-switch recombination in antibody secreting cells in response to a T-dependent antigen; B cells fail to undergo class-switch recombination to IgG3 or IgG1 in the presence of LPS or LPS plus IL-4, respectively   (MGI Ref ID J:114881)
      • however, well-formed germinal centers are observed in spleen after immunization   (MGI Ref ID J:114881)
    • decreased IgG level
      • decrease in IgG after TNP-OVA immunization   (MGI Ref ID J:114881)
    • increased B cell apoptosis
      • cultured B cells show increased apoptosis   (MGI Ref ID J:83213)
    • increased B cell proliferation
      • B cells are hyperproliferative in response to mitogenic stimuli and exhibit a lower threshold for activation through the B cell antigen receptor   (MGI Ref ID J:83213)
      • B cells exhibit altered cell cycle progression, with an increase in the percentage of cells in S and G2-M stages   (MGI Ref ID J:83213)
      • neonatal B cells proliferate strongly in response to both LPS and anti-IgM F(ab')2 unlike wild-type B cells which show a modest proliferation in response to LPS and no proliferation in response to the anti-IgM F(ab')2   (MGI Ref ID J:155314)
    • increased IgM level
      • increase in IgM after TNP-OVA immunization   (MGI Ref ID J:114881)
  • abnormal plasma cell morphology
    • increase in numbers of IgMhi antibody secreting cells and decrease in numbers of IgGhi antibody secreting cells   (MGI Ref ID J:114881)
  • decreased spleen germinal center number
    • reduction in germinal center formation in response to sheep red blood cell immunization and in response to environmental antigens   (MGI Ref ID J:83213)
  • increased B cell number
    • increase in the absolute number of splenic B cells, attributed mainly to the expansion/accumulation of MZ B cells   (MGI Ref ID J:83213)
    • increased B-1 B cell number
      • expansion of the B1 cell population   (MGI Ref ID J:83213)
    • increased marginal zone B cell number
      • expansion of the MZ B cell compartment   (MGI Ref ID J:83213)
  • cellular phenotype
  • increased B cell apoptosis
    • cultured B cells show increased apoptosis   (MGI Ref ID J:83213)

Cd19tm1(cre)Cgn/Cd19tm1(cre)Cgn Ptentm1Hwu/Ptentm1Hwu

        involves: 129P2/OlaHsd * 129S4/SvJae   (conditional)
  • immune system phenotype
  • *normal* immune system phenotype
    • the population of B1 and MZ B cells that are absent in single homozygous CD19 mutants is restored   (MGI Ref ID J:83213)
    • mutants are capable of forming germinal centers when immunized with sheep red blood cells   (MGI Ref ID J:83213)

Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+ Ptentm1Hwu/Ptentm1Hwu

        involves: 129 * 129S4/SvJae * BALB/c * C57BL/6   (conditional)
  • mortality/aging
  • premature death
    • most females that develop lymphomas die at about 9 weeks post-4OHT injection   (MGI Ref ID J:130367)
    • all mutants die from tumor burden by 45 weeks post-4OHT injection   (MGI Ref ID J:130367)
  • tumorigenesis
  • increased tumor incidence
    • treatment of mice with 4OHT at 6 weeks of age to induce cre-mediated recombination results in tumor formation with a mean latency of 17 weeks   (MGI Ref ID J:130367)
    • multiple tumors are seen in 27.3% of 4OHT-treated mice   (MGI Ref ID J:130367)
    • 46.1% of females develop endometrial cancer after 4OHT treatment   (MGI Ref ID J:130367)
    • increased T cell derived lymphoma incidence
      • 76.9% incidence of lymphomas in females after 4OHT treatment   (MGI Ref ID J:130367)
      • 40% incidence of lymphomas in males after 4OHT treatment   (MGI Ref ID J:130367)
      • lymphomas mainly arise from the thymus and mesenteric lymph nodes   (MGI Ref ID J:130367)
      • all lymphomas are derived from CD3+ T-cells with either a mature appearance of small lymphocytes or large lymphoblasts   (MGI Ref ID J:130367)
    • increased gastrointestinal tumor incidence
      • 35% of males develop intestinal cancer after 4OHT treatment, arising from the colorectum and small intestine   (MGI Ref ID J:130367)
    • increased incidence of tumors by chemical induction
      • about 50% of males and females exhibit malignant tumors at 21 weeks and 10-11 weeks after 4OHT treatment, respectively   (MGI Ref ID J:130367)
    • increased prostate gland tumor incidence
      • 20% of males develop prostate cancer after 4OHT treatment   (MGI Ref ID J:130367)
      • increased prostate intraepithelial neoplasia incidence
        • prostate intraepithelial neoplasm (PIN) is observed at 4-6 weeks post 4-OHT treatment   (MGI Ref ID J:130367)
    • increased skin squamous cell carcinoma incidence
      • 10% of males and 15.4% of females develop squamous cell carcinoma of the epidermis after 4OHT treatment   (MGI Ref ID J:130367)
  • digestive/alimentary phenotype
  • intestine polyps
    • males develop small or large intestinal polyps at more than 35 weeks post 4OHT treatment   (MGI Ref ID J:130367)
  • endocrine/exocrine gland phenotype
  • prostate gland hyperplasia
    • prostate hyperplasia is observed at 4-6 weeks post 4-OHT treatment   (MGI Ref ID J:130367)
  • reproductive system phenotype
  • endometrium hyperplasia
    • most females develop endometrial hyperplasia at between 7 and 9 weeks post 4-OHT treatment   (MGI Ref ID J:130367)
  • prostate gland hyperplasia
    • prostate hyperplasia is observed at 4-6 weeks post 4-OHT treatment   (MGI Ref ID J:130367)
  • integument phenotype
  • increased skin squamous cell carcinoma incidence
    • 10% of males and 15.4% of females develop squamous cell carcinoma of the epidermis after 4OHT treatment   (MGI Ref ID J:130367)
  • homeostasis/metabolism phenotype
  • increased incidence of tumors by chemical induction
    • about 50% of males and females exhibit malignant tumors at 21 weeks and 10-11 weeks after 4OHT treatment, respectively   (MGI Ref ID J:130367)

Ptentm1Hwu/Pten+ Tg(Nkx2-1-cre)2Sand/0

        involves: 129S4/SvJae * BALB/c * C57BL/6   (conditional)
  • endocrine/exocrine gland phenotype
  • abnormal thyroid follicle morphology
    • enlarged follicles   (MGI Ref ID J:197590)
  • enlarged thyroid gland
    • mutants have an enlarged thyroid at 2 years of age and exhibit a goiter-like phenotype, but do not show development of tumors   (MGI Ref ID J:197590)
    • thyroid gland hyperplasia   (MGI Ref ID J:197590)
  • homeostasis/metabolism phenotype
  • increased thyroxine level
    • P14 mutants show an increase in T4 levels   (MGI Ref ID J:197590)

Ptentm1Hwu/Pten+ Tg(Nkx2-1-cre)2Sand/0

        B6.Cg-Ptentm1Hwu Tg(Nkx2-1-cre)2Sand   (conditional)
  • endocrine/exocrine gland phenotype
  • abnormal thyroid gland morphology
    • altered thyroid structure with normal areas that include colloid-filled follicles and normal areas with focal hyperplasia, polynuclear cells, small nonencapsulated areas of hypercellularity with solid and/or mircofollicular patterns and internal hemorrhage   (MGI Ref ID J:197590)
  • homeostasis/metabolism phenotype
  • decreased thyroxine level
    • P14 mutants show a mild decrease of T4 but normal TSH   (MGI Ref ID J:197590)
  • tumorigenesis
  • increased thyroid tumor incidence
    • 100% of mutants develop differentiated follicular tumors of the thyroid after about 2 years of age   (MGI Ref ID J:197590)

Ptentm1Hwu/Ptentm1Hwu Lyz2tm1(cre)Ifo/Lyz2+

        involves: 129P2/OlaHsd * 129S4/SvJae   (conditional)
  • immune system phenotype
  • abnormal alveolar macrophage morphology
    • number of resident alveolar macrophages in unchallenged mutants is increased by more than 60% percent compared to wild-type   (MGI Ref ID J:148947)
  • abnormal cytokine level
    • increase in cytokine/chemokine concentrations in inflamed lungs of E.coli infected mutants due to increased numbers of resident alveolar macrophages and not due to enhanced capability of macrophages to produce cytokines or chemokines   (MGI Ref ID J:148947)
  • abnormal macrophage chemotaxis
    • macrophage recruitment to inflamed lungs is increased   (MGI Ref ID J:148947)
  • abnormal neutrophil physiology
    • neutrophils isolated from bone marrow live longer than wild-type neutrophils   (MGI Ref ID J:114699)
    • neutrophils exhibit enhanced ruffling in response to the chemoattractant fMLP or IL-8   (MGI Ref ID J:145331)
    • polarized neutrophils exhibit a considerable increase in multiple pseudopodia compared to wild-type mice   (MGI Ref ID J:145331)
    • neutrophils show more diffuse F-actin localization at the leading edge or pseudopodia than wild-type neutrophils   (MGI Ref ID J:145331)
    • fMLP-stimulated, but not PMA-stimulated, neutrophils exhibit increased and prolonged superoxide production compared to wild-type neutrophils   (MGI Ref ID J:145331)
    • neutrophils exhibit enhanced transwell chemotaxis toward fMLP, IL-8 or C5a   (MGI Ref ID J:145331)
    • neutrophils are more active and move faster than wild-type neutrophils but lack some of the directionality of wild-type neutrophils   (MGI Ref ID J:145331)
    • in a model of peritonitis, neutrophil recruitment at sites of inflammation is increased in mutants compared to wild-type mice   (MGI Ref ID J:145331)
    • in a model of bacterial pneumonia, apoptosis of lung recruited neutrophils is reduced in mutants compared to wild-type mice   (MGI Ref ID J:148947)
    • neutrophils exhibit enhanced bacteria-killing capacity in a model of bacterial pneumonia   (MGI Ref ID J:148947)
    • neutrophils have an increased phagocytic index compared to wild-type in a model of bacterial pneumonia   (MGI Ref ID J:148947)
    • neutrophils exhibit enhanced E.coli and zymosan-induced phagocytosis-associated superoxide production   (MGI Ref ID J:148947)
    • impaired neutrophil recruitment
      • in a bacterial pneumonia model in which mutants are intratracheally infected with E.coli to induce lung inflammation, mutants exhibit an increase in bacteria-induced neutrophil recruitment compared to controls   (MGI Ref ID J:148947)
      • mutants treated with the chemotherapeutic drug, cyclophosphamide, to induce neutropenia, exhibit fewer neutrophils in the lungs than untreated mutants, but more neutrophils than drug treated wild-type mice   (MGI Ref ID J:148947)
  • decreased susceptibility to bacterial infection
    • induction of neutropenia in mutants with the chemotherapeutic drug, cyclophosphamide, results in enhanced neutrophil accumulation in the lungs leading to better clearance of instilled bacteria and accelerated resolution of bacteria-induced lung inflammation   (MGI Ref ID J:148947)
    • decreased susceptibility to bacterial infection induced morbidity/mortality
      • mutants made neutropenic with the chemotherapeutic drug, cyclophosphamide, exhibit decreased mortality after E.coli challenge compared to wild-type mice due to enhanced neutrophil accumulation in the lungs (50% survival for mutants compared to 7% survival for wild-type mice)   (MGI Ref ID J:148947)
  • increased susceptibility to bacterial infection
    • mutants intratracheally infected with E.coli exhibit increased neutrophil recruitment to lungs and increased lung inflammation, pulmonary edema, and increased susceptibility to death compared to controls   (MGI Ref ID J:148947)
    • increased susceptibility to bacterial infection induced morbidity/mortality
      • mutants exhibit an increase in pneumonia-associated death rate compared to wild-type mice, with only 50% of mutants surviving compared to 80% survival of wild-type mice   (MGI Ref ID J:148947)
  • lung inflammation
    • mutants develop more severe lung inflammation in response to bacterial pneumonia than controls   (MGI Ref ID J:148947)
  • hematopoietic system phenotype
  • abnormal alveolar macrophage morphology
    • number of resident alveolar macrophages in unchallenged mutants is increased by more than 60% percent compared to wild-type   (MGI Ref ID J:148947)
  • abnormal macrophage chemotaxis
    • macrophage recruitment to inflamed lungs is increased   (MGI Ref ID J:148947)
  • abnormal neutrophil physiology
    • neutrophils isolated from bone marrow live longer than wild-type neutrophils   (MGI Ref ID J:114699)
    • neutrophils exhibit enhanced ruffling in response to the chemoattractant fMLP or IL-8   (MGI Ref ID J:145331)
    • polarized neutrophils exhibit a considerable increase in multiple pseudopodia compared to wild-type mice   (MGI Ref ID J:145331)
    • neutrophils show more diffuse F-actin localization at the leading edge or pseudopodia than wild-type neutrophils   (MGI Ref ID J:145331)
    • fMLP-stimulated, but not PMA-stimulated, neutrophils exhibit increased and prolonged superoxide production compared to wild-type neutrophils   (MGI Ref ID J:145331)
    • neutrophils exhibit enhanced transwell chemotaxis toward fMLP, IL-8 or C5a   (MGI Ref ID J:145331)
    • neutrophils are more active and move faster than wild-type neutrophils but lack some of the directionality of wild-type neutrophils   (MGI Ref ID J:145331)
    • in a model of peritonitis, neutrophil recruitment at sites of inflammation is increased in mutants compared to wild-type mice   (MGI Ref ID J:145331)
    • in a model of bacterial pneumonia, apoptosis of lung recruited neutrophils is reduced in mutants compared to wild-type mice   (MGI Ref ID J:148947)
    • neutrophils exhibit enhanced bacteria-killing capacity in a model of bacterial pneumonia   (MGI Ref ID J:148947)
    • neutrophils have an increased phagocytic index compared to wild-type in a model of bacterial pneumonia   (MGI Ref ID J:148947)
    • neutrophils exhibit enhanced E.coli and zymosan-induced phagocytosis-associated superoxide production   (MGI Ref ID J:148947)
    • impaired neutrophil recruitment
      • in a bacterial pneumonia model in which mutants are intratracheally infected with E.coli to induce lung inflammation, mutants exhibit an increase in bacteria-induced neutrophil recruitment compared to controls   (MGI Ref ID J:148947)
      • mutants treated with the chemotherapeutic drug, cyclophosphamide, to induce neutropenia, exhibit fewer neutrophils in the lungs than untreated mutants, but more neutrophils than drug treated wild-type mice   (MGI Ref ID J:148947)
  • homeostasis/metabolism phenotype
  • abnormal cytokine level
    • increase in cytokine/chemokine concentrations in inflamed lungs of E.coli infected mutants due to increased numbers of resident alveolar macrophages and not due to enhanced capability of macrophages to produce cytokines or chemokines   (MGI Ref ID J:148947)
  • pulmonary edema
    • increased neutrophil recruitment to lungs leads to pulmonary edema formation and increased protein accumulation   (MGI Ref ID J:148947)
  • mortality/aging
  • decreased susceptibility to bacterial infection induced morbidity/mortality
    • mutants made neutropenic with the chemotherapeutic drug, cyclophosphamide, exhibit decreased mortality after E.coli challenge compared to wild-type mice due to enhanced neutrophil accumulation in the lungs (50% survival for mutants compared to 7% survival for wild-type mice)   (MGI Ref ID J:148947)
  • increased susceptibility to bacterial infection induced morbidity/mortality
    • mutants exhibit an increase in pneumonia-associated death rate compared to wild-type mice, with only 50% of mutants surviving compared to 80% survival of wild-type mice   (MGI Ref ID J:148947)
  • respiratory system phenotype
  • abnormal alveolar macrophage morphology
    • number of resident alveolar macrophages in unchallenged mutants is increased by more than 60% percent compared to wild-type   (MGI Ref ID J:148947)
  • lung inflammation
    • mutants develop more severe lung inflammation in response to bacterial pneumonia than controls   (MGI Ref ID J:148947)
  • pulmonary edema
    • increased neutrophil recruitment to lungs leads to pulmonary edema formation and increased protein accumulation   (MGI Ref ID J:148947)
  • cellular phenotype
  • abnormal macrophage chemotaxis
    • macrophage recruitment to inflamed lungs is increased   (MGI Ref ID J:148947)

Ptentm1Hwu/Ptentm1Hwu Tg(Alb-cre)21Mgn/0

        involves: 129S4/SvJae * C57BL/6 * DBA   (conditional)
  • liver/biliary system phenotype
  • enlarged liver   (MGI Ref ID J:88441)
    • mutants exhibit enlarged, whitish livers containing large fat vacuoles by 12 weeks of age   (MGI Ref ID J:171445)
    • mutants treated with rapamycin show reduced hepatocyte cell size, thus reducing the liver:body weight ratio   (MGI Ref ID J:171445)
    • increased liver weight   (MGI Ref ID J:160759)
  • hepatic steatosis   (MGI Ref ID J:160759)
    • progressive development of fatty liver   (MGI Ref ID J:88441)
    • mutants exhibit enlarged, whitish livers containing large fat vacuoles by 12 weeks of age   (MGI Ref ID J:171445)
    • mutants treated with rapamycin exhibit no differences in steatosis compared to vehicle-treated mutants   (MGI Ref ID J:171445)
  • increased liver triglyceride level
    • 2-4-fold increase of triglyceride content in the liver of 1 and 3 month old mutants, respectively   (MGI Ref ID J:160759)
    • mutants exhibit elevated hepatic triglyceride levels   (MGI Ref ID J:171445)
    • mutants treated with rapamycin exhibit no differences in steatosis or triglyceride levels compared to vehicle-treated mutants, however the average hepatocyte cell size was reduced, thus reducing the liver:body weight   (MGI Ref ID J:171445)
  • pale liver   (MGI Ref ID J:88441)
  • adipose tissue phenotype
  • decreased total body fat amount
    • 50% reduction in total body fat content   (MGI Ref ID J:88441)
  • homeostasis/metabolism phenotype
  • abnormal fatty acid level
    • hepatocyte fatty acid uptake by passive diffusion is increased by 20% compared to controls, however active transportation of fatty acid is not changed and thus total fatty acid uptake is not significantly altered   (MGI Ref ID J:88441)
    • rate of fatty acid synthesis is 2.5-fold higher in mutant livers than in controls   (MGI Ref ID J:88441)
    • decreased circulating free fatty acid level
      • 30% decrease in circulating free fatty acids   (MGI Ref ID J:88441)
  • decreased circulating glucose level
    • decrease in fasting glucose levels at 1 and 3 months of age, however at 6 months of age, when severe steatosis is seen, the fasting glucose level is similar to wild-type   (MGI Ref ID J:88441)
  • decreased circulating insulin level
    • decrease in fasting plasma insulin levels at 3 and 6 months of age   (MGI Ref ID J:88441)
  • decreased circulating leptin level
    • decrease in serum leptin levels at one month of age   (MGI Ref ID J:88441)
    • however eating behavior is normal   (MGI Ref ID J:88441)
  • impaired lipolysis
    • decrease in lipolysis rate   (MGI Ref ID J:88441)
  • improved glucose tolerance
    • increase in glucose clearance during an intraperitoneal glucose load   (MGI Ref ID J:88441)
  • increased glycogen level
    • increase in glycogen storage in the liver   (MGI Ref ID J:88441)
  • increased insulin sensitivity
    • increase in insulin sensitivity in the liver   (MGI Ref ID J:88441)
  • increased triglyceride level
    • 3-fold increase in triglyceride content in the liver   (MGI Ref ID J:88441)
    • however, normal levels of plasma triglycerides   (MGI Ref ID J:88441)
    • increased liver triglyceride level
      • 2-4-fold increase of triglyceride content in the liver of 1 and 3 month old mutants, respectively   (MGI Ref ID J:160759)
      • mutants exhibit elevated hepatic triglyceride levels   (MGI Ref ID J:171445)
      • mutants treated with rapamycin exhibit no differences in steatosis or triglyceride levels compared to vehicle-treated mutants, however the average hepatocyte cell size was reduced, thus reducing the liver:body weight   (MGI Ref ID J:171445)
  • growth/size/body phenotype
  • decreased total body fat amount
    • 50% reduction in total body fat content   (MGI Ref ID J:88441)

Ptentm1Hwu/Ptentm1Hwu Tg(Cdh16-cre)91Igr/0

        involves: 129S4/SvJae * ICR   (conditional)
  • endocrine/exocrine gland phenotype
  • abnormal seminal vesicle morphology
    • epithelial hyperplasia in vesicular glands   (MGI Ref ID J:137442)
  • reproductive system phenotype
  • abnormal reproductive system morphology
    • genital tissues are enlarged   (MGI Ref ID J:137442)
    • abnormal endometrium morphology
      • endometrial hyperplasia is accompanied by partial squamous differentiation   (MGI Ref ID J:137442)
      • endometrium hyperplasia
        • hyperplasia of the endometrial glands and lumen   (MGI Ref ID J:137442)
    • abnormal epididymis epithelium morphology
      • epithelial hyperplasia in epididymis   (MGI Ref ID J:137442)
    • abnormal seminal vesicle morphology
      • epithelial hyperplasia in vesicular glands   (MGI Ref ID J:137442)
    • abnormal vas deferens morphology
      • epithelial hyperplasia in vas deferens   (MGI Ref ID J:137442)
  • tumorigenesis
  • *normal* tumorigenesis
    • mice up to 1 year of age do not form tumors   (MGI Ref ID J:137442)

Ptentm1Hwu/Ptentm1Hwu Tg(Cdh16-cre)91Igr/0

        involves: 129S4/SvJae * BALB/c * C57BL/6J * ICR   (conditional)
  • renal/urinary system phenotype
  • *normal* renal/urinary system phenotype
    • mutants do not develop hydronephrosis   (MGI Ref ID J:137073)
    • abnormal ureter morphology
      • hyperproliferation and enlarged epithelial cells in the ureter   (MGI Ref ID J:137073)
    • abnormal urinary bladder urothelium morphology
      • hyperproliferation and enlarged epithelial cells in the bladder   (MGI Ref ID J:137073)

Ptentm1Hwu/Ptentm1Hwu Tg(Cdh5-cre)7Mlia/0

        involves: 129S4/SvJae * BALB/c * C57BL/6 * FVB/N   (conditional)
  • hematopoietic system phenotype
  • abnormal hematopoiesis
    • progressive development of myeloproliferative disorder and leukemogenesis in the chronic phase followed by blast crisis   (MGI Ref ID J:135172)
    • increased leukocyte cell number
      • 2-3 months after birth, mutants show increased circulating neutrophils and white blood cells and leukemic blast invasion into hematopoietic and non-hematopoietic organs   (MGI Ref ID J:135172)
      • increased neutrophil cell number
        • one month after birth, mutants develop a myeloid shift with increased neutrophil counts   (MGI Ref ID J:135172)
  • enlarged spleen
  • enlarged thymus
    • 70% of mutants exhibit enlarged thymus   (MGI Ref ID J:135172)
  • immune system phenotype
  • enlarged lymph nodes
    • 70% of mutants exhibit enlarged lymph nodes   (MGI Ref ID J:135172)
  • enlarged spleen
  • enlarged thymus
    • 70% of mutants exhibit enlarged thymus   (MGI Ref ID J:135172)
  • increased leukocyte cell number
    • 2-3 months after birth, mutants show increased circulating neutrophils and white blood cells and leukemic blast invasion into hematopoietic and non-hematopoietic organs   (MGI Ref ID J:135172)
    • increased neutrophil cell number
      • one month after birth, mutants develop a myeloid shift with increased neutrophil counts   (MGI Ref ID J:135172)
  • liver/biliary system phenotype
  • enlarged liver
  • tumorigenesis
  • increased acute lymphoblastic leukemia incidence
    • 74% of mutants develop T-lymphoblastic leukemia   (MGI Ref ID J:135172)
  • increased acute promyelocytic leukemia incidence
    • 26% of mutants develop acute myeloid leukemia   (MGI Ref ID J:135172)
  • endocrine/exocrine gland phenotype
  • enlarged thymus
    • 70% of mutants exhibit enlarged thymus   (MGI Ref ID J:135172)

Ptentm1Hwu/Ptentm1Hwu Tg(Ckmm-cre)5Khn/?

        involves: 129S4/SvJae * FVB   (conditional)
  • muscle phenotype
  • abnormal muscle regeneration
    • in mice fed a normal diet, the weights of injured tibialis anterior muscles are greater than weights of muscles in controls   (MGI Ref ID J:169364)
    • regenerating myofibers after injury are larger compared to control injured myofibers, indicating that mutants exhibit a promotion in regeneration of injured muscles   (MGI Ref ID J:169364)
    • after 8 months of a high-fat diet, mutants exhibit larger myofiber sizes of regenerating muscles at 6 and 12 days after injury and increased weights of the injured tibialis anterior muscles than controls   (MGI Ref ID J:169364)
    • after 8 months on a high-fat diet, collagen deposition is reduced in regenerating muscles compared to controls   (MGI Ref ID J:169364)
  • homeostasis/metabolism phenotype
  • decreased circulating glucose level
    • after 8 months of a high-fat diet, mutants exhibit lower glucose levels than controls on the same diet   (MGI Ref ID J:169364)
  • decreased circulating insulin level
    • after 8 months of a high-fat diet, mutants exhibit lower insulin levels than controls on the same diet   (MGI Ref ID J:169364)

Ptentm1Hwu/Ptentm1Hwu Tg(Cr2-cre)3Cgn/0

        involves: 129S4/SvJae   (conditional)
  • mortality/aging
  • complete preweaning lethality
    • no time point given   (MGI Ref ID J:157297)

Ptentm1Hwu/Ptentm1Hwu Tg(Ddx4-cre)1Dcas/0

        involves: 129S4/SvJae * FVB/N   (conditional)
  • endocrine/exocrine gland phenotype
  • abnormal ovary physiology
    • ovaries explanted at birth and cultured for 8 days grow more rapidly than controls   (MGI Ref ID J:138697)
  • enlarged ovary
    • ovaries are enlarged by P21 due to global primordial follicle activation   (MGI Ref ID J:138697)
  • reproductive system phenotype
  • abnormal ovary physiology
    • ovaries explanted at birth and cultured for 8 days grow more rapidly than controls   (MGI Ref ID J:138697)
  • enlarged ovary
    • ovaries are enlarged by P21 due to global primordial follicle activation   (MGI Ref ID J:138697)
  • reduced female fertility
    • females exhibit a dramatic age-dependent decrease in fertility and have no more than two litters   (MGI Ref ID J:138697)

Ptentm1Hwu/Ptentm1Hwu Tg(GFAP-cre)25Mes/0

        involves: 129S4/SvJae * FVB/N   (conditional)
  • mortality/aging
  • complete lethality at weaning
    • death occurs around P21   (MGI Ref ID J:100428)
  • nervous system phenotype
  • abnormal cerebellar Purkinje cell layer
    • Purkinje layer defect is first seen at P4-P6 and by P9, numerous Purkinje neurons are randomly scattered   (MGI Ref ID J:100428)
    • abnormal Bergmann glial cell morphology
      • disruption of Bergmann glial layering   (MGI Ref ID J:100428)
      • abnormal Bergmann glial cell differentiation
        • premature differentiation of Bergmann glia leading to extensive layering defects   (MGI Ref ID J:100428)
      • ectopic Bergmann glia cells
        • some Bergmann cell bodies are randomly distributed at P7 and lose their contacts to the pial surface and are positioned deep within the internal granule layer region   (MGI Ref ID J:100428)
    • ectopic Purkinje cell
      • Purkinje cell layer is normal at P3 but there are many ectopic Purkinje cells by P9   (MGI Ref ID J:100428)
  • abnormal cerebellar granule layer morphology
    • lack of an organized internal granule layer (IGL) at P6   (MGI Ref ID J:100428)
    • severe granule neuron layering defects   (MGI Ref ID J:100428)
    • abnormal cerebellar granule cell morphology
      • mutants exhibit granule neuron migration defects, with granule neurons failing to migrate to the internal granule layer and accumulating in the molecular layer (ML)   (MGI Ref ID J:100428)
      • granule neurons are resistant to low potassium-induced cell death under serum deprivation conditions   (MGI Ref ID J:100428)
  • abnormal cerebellum development
    • cerebella layering defects   (MGI Ref ID J:100428)
    • before P3, cerebella are enlarged but the external granule layer (EGL) and cerebellar lobules are normal and Purkinje cell position is normal   (MGI Ref ID J:100428)
    • however, after P6, mutants show a marked cerebellar enlargement and lack internal granule layer and folia   (MGI Ref ID J:100428)
    • abnormal cerebellar foliation
      • loss of foliation after P6   (MGI Ref ID J:100428)
  • enlarged cerebellum   (MGI Ref ID J:100428)
  • increased brain size   (MGI Ref ID J:100428)
  • cellular phenotype
  • abnormal Bergmann glial cell differentiation
    • premature differentiation of Bergmann glia leading to extensive layering defects   (MGI Ref ID J:100428)
  • growth/size/body phenotype
  • megacephaly   (MGI Ref ID J:100428)

Ptentm1Hwu/Ptentm1Hwu Tg(GZMB-cre)1Jcb/0

        involves: 129S4/SvJae * FVB/N   (conditional)
  • immune system phenotype
  • abnormal CD8-positive T cell physiology
    • mutants infected with lymphocytic choriomeningitis virus (LCMV) to induce T-cell activation and thus cre-expression exhibit better survival of effector CD8 T cells under serum-starvation conditions compared to controls, but only show modest effects on the expansion and contraction of effector CD8 T cells   (MGI Ref ID J:164425)
    • clonal burst of mutant effector CD8 T cells is about 1/2 that of wild-type controls and there is a slight, but not significant reduction in the number of memory T cells that form in lymphoid and nonlymphoid tissues   (MGI Ref ID J:164425)
  • decreased interleukin-2 secretion
    • production of IL-2 by CD8 T cells is diminished in mutants infected with LCMV to induce T-cell activation and thus cre-expression   (MGI Ref ID J:164425)
  • hematopoietic system phenotype
  • abnormal CD8-positive T cell physiology
    • mutants infected with lymphocytic choriomeningitis virus (LCMV) to induce T-cell activation and thus cre-expression exhibit better survival of effector CD8 T cells under serum-starvation conditions compared to controls, but only show modest effects on the expansion and contraction of effector CD8 T cells   (MGI Ref ID J:164425)
    • clonal burst of mutant effector CD8 T cells is about 1/2 that of wild-type controls and there is a slight, but not significant reduction in the number of memory T cells that form in lymphoid and nonlymphoid tissues   (MGI Ref ID J:164425)

Ptentm1Hwu/Ptentm1Hwu Tg(Gdf9-cre)5092Coo/0

        B6.Cg-Ptentm1Hwu Tg(Gdf9-cre)5092Coo   (conditional)
  • endocrine/exocrine gland phenotype
  • abnormal corpus luteum morphology
    • luteolysis is observed (degeneration of corpora lutea) at 12 weeks of age   (MGI Ref ID J:131827)
  • abnormal ovarian follicle morphology
    • at P8, ovaries appear larger with more activated follicles, including transient follicles containing enlarged oocytes surrounded by flattened pregranulosa cells, primary follicles with enlarged oocytes surrounded by one layer of cuboidal granulosa cells and some secondary follicles with two layers of granulosa cells   (MGI Ref ID J:131827)
    • follicular structure at 12 weeks of age is deformed and luteolysis is observed   (MGI Ref ID J:131827)
    • reduction in follicle death and clearance before and around the time of sexual maturity   (MGI Ref ID J:131827)
    • at 7 weeks of age, ovaries show increased numbers of transient and preantral type 5 follicles   (MGI Ref ID J:131827)
    • abnormal ovarian folliculogenesis
      • growth dynamics of activated transient follicles is different than in controls, with some follicles remaining at the transient stage whereas others develop further   (MGI Ref ID J:131827)
    • abnormal primordial ovarian follicle morphology
      • premature activation of the primordial follicle pool resulting in depletion of primordial follicles in early adulthood   (MGI Ref ID J:131827)
      • percentage of primordial follicles in ovaries at P8 is lower (49.6%) than in controls (83.6%)   (MGI Ref ID J:131827)
      • by p23, no primordial follicles an be identified in mutants compared to 69.2% of follicles in controls areas are still at the primordial stage   (MGI Ref ID J:131827)
  • enlarged ovary
    • at P8, ovaries appear larger with more activated follicles   (MGI Ref ID J:131827)
    • by P23 and 35, ovaries remain larger and contain more activated follicles   (MGI Ref ID J:131827)
  • homeostasis/metabolism phenotype
  • increased follicle stimulating hormone level
    • increase in levels of follicle-stimulating hormone at 12-20-week old females   (MGI Ref ID J:131827)
  • increased luteinizing hormone level
    • increase in levels of luteinizing hormone at 12-20-week old females   (MGI Ref ID J:131827)
  • reproductive system phenotype
  • abnormal corpus luteum morphology
    • luteolysis is observed (degeneration of corpora lutea) at 12 weeks of age   (MGI Ref ID J:131827)
  • abnormal female reproductive system physiology
    • females exhibit activation of the pool of primordial follicles that leads to follicle depletion, causing premature ovarian failure   (MGI Ref ID J:131827)
    • many transient follicles contain degraded oocytes suggesting that some prematurely activated follicles undergo atresia   (MGI Ref ID J:131827)
    • abnormal estrous cycle
      • older females exhibit irregular estrous cycles   (MGI Ref ID J:131827)
    • female infertility
      • females become infertile in early adulthood, after 12-13 weeks of age   (MGI Ref ID J:131827)
  • abnormal oocyte morphology
    • accelerated oocyte growth   (MGI Ref ID J:131827)
    • many transient follicles contain degraded oocytes   (MGI Ref ID J:131827)
  • abnormal ovarian follicle morphology
    • at P8, ovaries appear larger with more activated follicles, including transient follicles containing enlarged oocytes surrounded by flattened pregranulosa cells, primary follicles with enlarged oocytes surrounded by one layer of cuboidal granulosa cells and some secondary follicles with two layers of granulosa cells   (MGI Ref ID J:131827)
    • follicular structure at 12 weeks of age is deformed and luteolysis is observed   (MGI Ref ID J:131827)
    • reduction in follicle death and clearance before and around the time of sexual maturity   (MGI Ref ID J:131827)
    • at 7 weeks of age, ovaries show increased numbers of transient and preantral type 5 follicles   (MGI Ref ID J:131827)
    • abnormal ovarian folliculogenesis
      • growth dynamics of activated transient follicles is different than in controls, with some follicles remaining at the transient stage whereas others develop further   (MGI Ref ID J:131827)
    • abnormal primordial ovarian follicle morphology
      • premature activation of the primordial follicle pool resulting in depletion of primordial follicles in early adulthood   (MGI Ref ID J:131827)
      • percentage of primordial follicles in ovaries at P8 is lower (49.6%) than in controls (83.6%)   (MGI Ref ID J:131827)
      • by p23, no primordial follicles an be identified in mutants compared to 69.2% of follicles in controls areas are still at the primordial stage   (MGI Ref ID J:131827)
  • enlarged ovary
    • at P8, ovaries appear larger with more activated follicles   (MGI Ref ID J:131827)
    • by P23 and 35, ovaries remain larger and contain more activated follicles   (MGI Ref ID J:131827)

Ptentm1Hwu/Ptentm1Hwu Tg(Gdf9-cre)5092Coo/0

        involves: 129S4/SvJae * C57BL/6   (conditional)
  • endocrine/exocrine gland phenotype
  • abnormal primordial ovarian follicle morphology
    • females exhibit prematurely activated primordial follicles (transient follicles with enlarged oocytes surrounded by flattened pre-granulosa cells) leading to complete depletion of follicles by 16 weeks of age   (MGI Ref ID J:151696)
  • reproductive system phenotype
  • abnormal primordial ovarian follicle morphology
    • females exhibit prematurely activated primordial follicles (transient follicles with enlarged oocytes surrounded by flattened pre-granulosa cells) leading to complete depletion of follicles by 16 weeks of age   (MGI Ref ID J:151696)

Ptentm1Hwu/Ptentm1Hwu Tg(Gdf9-cre)5092Coo/?

        involves: 129S4/SvJae * C57BL/6J   (conditional)
  • endocrine/exocrine gland phenotype
  • abnormal ovarian follicle morphology
    • mutant females exhibit accelerated activation of primordial follicles   (MGI Ref ID J:155357)
  • reproductive system phenotype
  • abnormal ovarian follicle morphology
    • mutant females exhibit accelerated activation of primordial follicles   (MGI Ref ID J:155357)

Ptentm1Hwu/Ptentm1Hwu Tg(Gfap-cre)77.6Mvs/0

        involves: 129S4/SvJae * BALB/c * C57BL/6NHsd   (conditional)
  • nervous system phenotype
  • abnormal neuron differentiation
    • cultured adult neural stem cells maintain their ability to differentiate into neurons for a longer time compared to wild-type cells   (MGI Ref ID J:146630)
    • increased neuronal precursor cell number
      • expansion of the adult neural stem cell and progenitor populations in the subependymal zone   (MGI Ref ID J:146630)
  • abnormal neuronal precursor proliferation
    • in culture, neurospheres formed by adult neural stem cells are generally larger and the stem cells' capacity for self renewal is prolonged compared to wild-type cells   (MGI Ref ID J:146630)
  • abnormal olfactory bulb morphology
    • continuous increase in the weight and size of the olfactory bulb compared to controls starting at 2.5 months of age   (MGI Ref ID J:146630)
    • the granule cell layer volume is increased 2 fold at 3.5 months of age   (MGI Ref ID J:146630)
    • the increase in volume is due to an increase in the number of cells migrating from the subependymal zone to the olfactory bulb and a decrease in the number of apoptotic cells in the granule cell layer   (MGI Ref ID J:146630)
  • abnormal postnatal subventricular zone morphology
    • increase in the volume of the subependymal zone compared to controls   (MGI Ref ID J:146630)
    • increase in the number of proliferating cells and DCX positive neuroblasts   (MGI Ref ID J:146630)
  • altered response to CNS ischemic injury
    • 7 days after induction of limited stroke in the sensorimotor cortex, mice have more neuroblasts in the peri-infarct cortex compared to controls   (MGI Ref ID J:146630)
    • however, there is no difference in the number of new cells present at 90 days after stroke induction   (MGI Ref ID J:146630)
  • behavior/neurological phenotype
  • abnormal response to novel odor
    • habituate faster to a novel odorant compared to controls   (MGI Ref ID J:146630)
    • however, no difference in response is seen on the first exposure to a novel odorant   (MGI Ref ID J:146630)
  • taste/olfaction phenotype
  • abnormal olfaction
    • mice recover olfactory ability more quickly following exposure to dichlobenil compared to controls   (MGI Ref ID J:146630)
  • tumorigenesis
  • *normal* tumorigenesis   (MGI Ref ID J:154673)
    • in contrast to other conditional null Pten genotypes no tumors are found in mice up to 2 years of age   (MGI Ref ID J:146630)
  • homeostasis/metabolism phenotype
  • altered response to CNS ischemic injury
    • 7 days after induction of limited stroke in the sensorimotor cortex, mice have more neuroblasts in the peri-infarct cortex compared to controls   (MGI Ref ID J:146630)
    • however, there is no difference in the number of new cells present at 90 days after stroke induction   (MGI Ref ID J:146630)
  • cellular phenotype
  • abnormal neuron differentiation
    • cultured adult neural stem cells maintain their ability to differentiate into neurons for a longer time compared to wild-type cells   (MGI Ref ID J:146630)
    • increased neuronal precursor cell number
      • expansion of the adult neural stem cell and progenitor populations in the subependymal zone   (MGI Ref ID J:146630)
  • abnormal neuronal precursor proliferation
    • in culture, neurospheres formed by adult neural stem cells are generally larger and the stem cells' capacity for self renewal is prolonged compared to wild-type cells   (MGI Ref ID J:146630)

Ptentm1Hwu/Ptentm1Hwu Tg(Ins2-cre)25Mgn/0

        involves: 129S4/SvJae * C57BL/6 * DBA   (conditional)
  • cellular phenotype
  • decreased cellular sensitivity to oxidative stress
    • islets are protected from oxidative stress   (MGI Ref ID J:106937)
  • endocrine/exocrine gland phenotype
  • abnormal pancreas physiology
    • decrease in apoptotic rate during pancreas remodeling at P17   (MGI Ref ID J:106937)
    • however, pancreas exhibits normal islet functions   (MGI Ref ID J:106937)
    • abnormal pancreatic beta cell physiology
      • increase in beta-cell proliferation at E17.5   (MGI Ref ID J:106937)
      • increased insulin secretion
        • after high-fat diet feeding, mutants maintain robust insulin secretion in response to glucose compared to controls which show attenuation of insulin secretion, indicating that mutant islets are protected against high-fat diet-induced beta-cell dysfunction   (MGI Ref ID J:170206)
  • abnormal pancreatic beta cell morphology
    • increase in beta cell size   (MGI Ref ID J:170206)
    • beta-cells maintain intact response to DNA-damaging stimuli unlike controls   (MGI Ref ID J:170206)
    • increased pancreatic beta cell mass
      • increase in beta cell mass, due to an increase in proliferation and in beta cell size   (MGI Ref ID J:170206)
      • however, mutants do not exhibit any further increase in beta-cell mass on a high-fat diet   (MGI Ref ID J:170206)
    • increased pancreatic beta cell number
      • number of insulin-producing cells is increased in islets   (MGI Ref ID J:106937)
  • enlarged pancreatic islets
    • 2-fold increase in islet size   (MGI Ref ID J:106937)
  • increased pancreatic islet number
    • 1.5-fold increase in islet numbers   (MGI Ref ID J:106937)
  • homeostasis/metabolism phenotype
  • *normal* homeostasis/metabolism phenotype
    • despite weight gain, mutants are protected from high-fat diet-induced diabetes, remaining euglycemic and showing improved glucose tolerance than controls on a high-fat diet   (MGI Ref ID J:170206)
    • decreased susceptibility to injury
      • mice are protected from STZ-induced beta-cell injury and diabetes   (MGI Ref ID J:106937)
    • hypoglycemia
      • hypoglycemia, however mice respond normally to a glucose challenge   (MGI Ref ID J:106937)
    • improved glucose tolerance
      • mutants are protected from high-fat diet-induced diabetes, remaining euglycemic and showing improved glucose tolerance than controls on a high-fat diet   (MGI Ref ID J:170206)
    • increased insulin secretion
      • after high-fat diet feeding, mutants maintain robust insulin secretion in response to glucose compared to controls which show attenuation of insulin secretion, indicating that mutant islets are protected against high-fat diet-induced beta-cell dysfunction   (MGI Ref ID J:170206)
    • increased insulin sensitivity
      • increase in peripheral insulin sensitivity   (MGI Ref ID J:170206)
  • growth/size/body phenotype
  • increased body weight   (MGI Ref ID J:170206)

Ptentm1Hwu/Ptentm1Hwu Tg(Ins2-cre)25Mgn/0

        involves: 129S4/SvJae * BALB/c * C57BL/6 * DBA   (conditional)
  • endocrine/exocrine gland phenotype
  • abnormal pancreatic beta cell morphology
    • beta-cell size is increased by 15% compared to controls   (MGI Ref ID J:170129)
    • number of proliferating beta-cells is increased by 34% compared to controls   (MGI Ref ID J:170129)
    • increased pancreatic beta cell mass
      • beta-cell mass is 86% higher than controls after adjusting for body size   (MGI Ref ID J:170129)
      • however, pancreatic insulin content is unchanged and insulin sensitivity is normal   (MGI Ref ID J:170129)
  • growth/size/body phenotype
  • postnatal growth retardation   (MGI Ref ID J:170129)

Ptentm1Hwu/Ptentm1Hwu Tg(MMTV-cre)4Mam/0

        involves: 129S4/SvJae * FVB   (conditional)
  • endocrine/exocrine gland phenotype
  • abnormal branching of the mammary ductal tree
    • virgin mammary ducts develop excessive side branches or small protrusions at 6 weeks of age   (MGI Ref ID J:78415)
  • abnormal involution of the mammary gland
    • delay in the normal involution process and a decrease in cell apoptosis   (MGI Ref ID J:78415)
  • abnormal mammary gland epithelium morphology
    • virgin mammary duct epithelium exhibits increased proliferation at 5 weeks and 14 weeks of age   (MGI Ref ID J:78415)
  • abnormal mammary gland growth during pregnancy
    • mammary glands exhibit much larger lobules on the 13th day of pregnancy   (MGI Ref ID J:78415)
  • abnormal mammary gland lobule morphology
    • virgin glands contain many lobuloalveolar buds which are normally seen during pregnancy indicating an acceleration in lobuloalveolar-like precocious differentiation   (MGI Ref ID J:78415)
  • mammary gland duct hyperplasia
    • mammary ducts grow much faster during puberty than in controls, leading to earlier occupancy of the fat pad and earlier disappearance of the terminal end buds than in controls   (MGI Ref ID J:78415)
  • mammary gland hyperplasia
    • mammary glands after one pregnancy show intra-luminal focal cellular hyperplasia and dysplasia   (MGI Ref ID J:78415)
  • reproductive system phenotype
  • abnormal mammary gland growth during pregnancy
    • mammary glands exhibit much larger lobules on the 13th day of pregnancy   (MGI Ref ID J:78415)
  • tumorigenesis
  • increased mammary gland tumor incidence
    • develop mammary gland tumors as early as 2 months of age   (MGI Ref ID J:78415)
    • tumor incidence is increased with shortened latencies in multiparous females   (MGI Ref ID J:78415)
    • increased fibroadenoma incidence
      • benign fibroadenomas   (MGI Ref ID J:78415)
    • increased mammary adenocarcinoma incidence
      • pleiomorphic adenocarcinomas   (MGI Ref ID J:78415)
  • integument phenotype
  • abnormal branching of the mammary ductal tree
    • virgin mammary ducts develop excessive side branches or small protrusions at 6 weeks of age   (MGI Ref ID J:78415)
  • abnormal involution of the mammary gland
    • delay in the normal involution process and a decrease in cell apoptosis   (MGI Ref ID J:78415)
  • abnormal mammary gland epithelium morphology
    • virgin mammary duct epithelium exhibits increased proliferation at 5 weeks and 14 weeks of age   (MGI Ref ID J:78415)
  • abnormal mammary gland growth during pregnancy
    • mammary glands exhibit much larger lobules on the 13th day of pregnancy   (MGI Ref ID J:78415)
  • abnormal mammary gland lobule morphology
    • virgin glands contain many lobuloalveolar buds which are normally seen during pregnancy indicating an acceleration in lobuloalveolar-like precocious differentiation   (MGI Ref ID J:78415)
  • mammary gland duct hyperplasia
    • mammary ducts grow much faster during puberty than in controls, leading to earlier occupancy of the fat pad and earlier disappearance of the terminal end buds than in controls   (MGI Ref ID J:78415)
  • mammary gland hyperplasia
    • mammary glands after one pregnancy show intra-luminal focal cellular hyperplasia and dysplasia   (MGI Ref ID J:78415)

Ptentm1Hwu/Ptentm1Hwu Tg(Mx1-cre)1Cgn/0

        involves: 129S4/SvJae * C57BL/6 * CBA   (conditional)
  • digestive/alimentary phenotype
  • intestine polyps
    • mice develop multiple polyps in the small intestine one month after completion of pIpC injection to induce Cre expression   (MGI Ref ID J:118329)
    • polyps show a large excess of crypt-like units at their base and aberrant positioning of crypts along the edges of villi   (MGI Ref ID J:118329)
    • overgrowth and insertions of stromal cells from the base of the polypoid mass are seen in the small intestine one month after completion of pIpC injection to induce Cre expression   (MGI Ref ID J:118329)
    • intestinal stem cells exhibit increased proliferation due to Akt activation and nuclear localization of beta-catenin resulting in an increase of intestinal stem cells in the crypts   (MGI Ref ID J:118329)
    • these excess stem cells initiate de novo crypt formation and crypt fission at a higher rate than in controls   (MGI Ref ID J:118329)
  • tumorigenesis
  • increased acute lymphoblastic leukemia incidence
    • mice injected with pIpC to induce Pten deletion, develop myeloproliferative disease and T-cell acute lymphoblastic leukemia   (MGI Ref ID J:169097)
  • immune system phenotype
  • enlarged spleen
    • mice injected with pIpC to induce Pten deletion have an enlarged spleen   (MGI Ref ID J:169097)
  • enlarged thymus
    • mice injected with pIpC to induce Pten deletion have an enlarged thymus   (MGI Ref ID J:169097)
  • mortality/aging
  • premature death
    • mean survival time of mice injected with pIpC to induce Pten deletion is 35 days   (MGI Ref ID J:169097)
  • hematopoietic system phenotype
  • enlarged spleen
    • mice injected with pIpC to induce Pten deletion have an enlarged spleen   (MGI Ref ID J:169097)
  • enlarged thymus
    • mice injected with pIpC to induce Pten deletion have an enlarged thymus   (MGI Ref ID J:169097)
  • endocrine/exocrine gland phenotype
  • enlarged thymus
    • mice injected with pIpC to induce Pten deletion have an enlarged thymus   (MGI Ref ID J:169097)

Ptentm1Hwu/Ptentm1Hwu Tg(Mx1-cre)1Cgn/0

        BKS.Cg-Ptprcb Thy1a Tg(Mx1-cre)1Cgn Ptentm1Hwu   (conditional)
  • mortality/aging
  • premature death
    • mutants become ill shortly after pIpC treatment and exhibit lethargy, ruffling of fur, and hunched posture and die from leukemia   (MGI Ref ID J:109085)
  • hematopoietic system phenotype
  • abnormal blood cell morphology/development
    • increase in blast cell frequency after pIpC administration to induce Cre expression   (MGI Ref ID J:109085)
    • extramedullary hematopoiesis
      • mice treated with polyinosine-polycytidine (pIpC) to induce Cre expression exhibit extramedullary hematopoiesis, with prominent expansion in the number of immature myeloid cells   (MGI Ref ID J:109085)
      • mice develop myeloproliferative disease shortly after pIpC administration to induce Cre expression with complete effacement of the splenic architecture   (MGI Ref ID J:109085)
  • abnormal hematopoietic stem cell physiology
    • mice treated with pIpC to induce Cre expression exhibit an increase in hematopoietic stem cell proliferation but become depleted, most likely due to inhibition of self-renewal as no increase in cell death was observed   (MGI Ref ID J:109085)
    • mutants maintained on rapamycin after pIpC treatment do not exhibit expansion of hematopoietic stem cells   (MGI Ref ID J:109085)
  • decreased bone marrow cell number
    • reduction in bone marrow cellularity after pIpC administration to induce Cre expression   (MGI Ref ID J:109085)
  • enlarged thymus
    • mice treated with pIpC to induce Cre expression exhibit an enlarged thymus   (MGI Ref ID J:109085)
  • spleen hyperplasia
    • 10-fold increase in spleen cellularity after pIpC administration to induce Cre expression   (MGI Ref ID J:109085)
  • immune system phenotype
  • enlarged thymus
    • mice treated with pIpC to induce Cre expression exhibit an enlarged thymus   (MGI Ref ID J:109085)
  • spleen hyperplasia
    • 10-fold increase in spleen cellularity after pIpC administration to induce Cre expression   (MGI Ref ID J:109085)
  • tumorigenesis
  • increased leukemia incidence
    • within 4-6 weeks after pIpC treatment, most mutants progress to leukemia, including acute myeloid leukemia and acute lymphoblastic leukemia   (MGI Ref ID J:109085)
    • mutants maintained on rapamycin after pIpC treatment do not develop leukemia   (MGI Ref ID J:109085)
    • increased acute lymphoblastic leukemia incidence
      • seen in mutants within 4-6 weeks after pIpC treatment   (MGI Ref ID J:109085)
    • increased acute promyelocytic leukemia incidence
      • seen in mutants within 4-6 weeks after pIpC treatment   (MGI Ref ID J:109085)
  • endocrine/exocrine gland phenotype
  • enlarged thymus
    • mice treated with pIpC to induce Cre expression exhibit an enlarged thymus   (MGI Ref ID J:109085)

Ptentm1Hwu/Ptentm1Hwu Tg(Mx1-cre)1Cgn/0

        involves: 129S4/SvJae * C57BL/6 * C57BL/6J * CBA   (conditional)
  • hematopoietic system phenotype
  • abnormal platelet activation
    • collagen-induced platelet activation is enhanced in mutants injected with poly(I:C) to induce cre expression   (MGI Ref ID J:165893)
    • increased platelet aggregation
      • platelets of mutants injected with poly(I:C) to induce cre expression are induced to aggregate by a much lower level of collagen than is required to induce the same response by wild-type platelets   (MGI Ref ID J:165893)
  • increased platelet cell number
    • mutants injected with poly(I:C) to induce cre expression, exhibit 25% more platelets in the blood than controls   (MGI Ref ID J:165893)
  • homeostasis/metabolism phenotype
  • abnormal platelet activation
    • collagen-induced platelet activation is enhanced in mutants injected with poly(I:C) to induce cre expression   (MGI Ref ID J:165893)
    • increased platelet aggregation
      • platelets of mutants injected with poly(I:C) to induce cre expression are induced to aggregate by a much lower level of collagen than is required to induce the same response by wild-type platelets   (MGI Ref ID J:165893)
  • decreased bleeding time
    • mutants injected with poly(I:C) to induce cre expression have an average bleeding time that is shorter than in controls   (MGI Ref ID J:165893)

Ptentm1Hwu/Ptentm1Hwu Tg(Myh6-cre/Esr1*)1Jmk/0

        involves: 129S4/SvJae * FVB/N   (conditional)
  • cardiovascular system phenotype
  • altered response to myocardial infarction
    • hearts of mutants treated with tamoxifen for 3 weeks to induce cre-expression develop significantly better function recovery in response to 30 min ischemia followed by 120 min reperfusion than controls, showing significantly improved end-diastolic pressure, left ventricle developed pressure (LVDP) and LVDP recoveries, and improved systolic and diastolic contractility of hearts   (MGI Ref ID J:149180)
    • at 60 min post reperfusion, recovery of left ventricular diastolic pressure reaches 77.9% of pre-ischemia in hearts versus 44% in controls   (MGI Ref ID J:149180)
    • hearts have significantly fewer apoptosis positive cardiomyocytes after ischemia/reperfusion (I/R) injury than controls   (MGI Ref ID J:149180)
    • decreased myocardial infarction size
      • mutants treated with tamoxifen to induce cre-expression exhibit a significant reduction in infarct size after ischemia   (MGI Ref ID J:149180)
  • homeostasis/metabolism phenotype
  • altered response to myocardial infarction
    • hearts of mutants treated with tamoxifen for 3 weeks to induce cre-expression develop significantly better function recovery in response to 30 min ischemia followed by 120 min reperfusion than controls, showing significantly improved end-diastolic pressure, left ventricle developed pressure (LVDP) and LVDP recoveries, and improved systolic and diastolic contractility of hearts   (MGI Ref ID J:149180)
    • at 60 min post reperfusion, recovery of left ventricular diastolic pressure reaches 77.9% of pre-ischemia in hearts versus 44% in controls   (MGI Ref ID J:149180)
    • hearts have significantly fewer apoptosis positive cardiomyocytes after ischemia/reperfusion (I/R) injury than controls   (MGI Ref ID J:149180)
    • decreased myocardial infarction size
      • mutants treated with tamoxifen to induce cre-expression exhibit a significant reduction in infarct size after ischemia   (MGI Ref ID J:149180)

Ptentm1Hwu/Ptentm1Hwu Tg(Nkx2-1-cre)2Sand/0

        involves: 129S4/SvJae * C57BL/6   (conditional)
  • respiratory system phenotype
  • increased Clara cell number
    • increase in the numbers of Clara cells in the lungs   (MGI Ref ID J:157922)

Ptentm1Hwu/Ptentm1Hwu Tg(Nkx2-1-cre)2Sand/0

        involves: 129S4/SvJae * BALB/c * C57BL/6   (conditional)
  • homeostasis/metabolism phenotype
  • *normal* homeostasis/metabolism phenotype
    • unlike on the congenic C57BL/6 background, mutants on the BALB/c background have normal T4 and TSH levels unlike on the congenic C57BL/6 background, mutants on the BALB/c background have normal T4 and TSH levels   (MGI Ref ID J:197590)
    • decreased susceptibility to injury
      • after naphthalene administration to induce lung injury, the proximal airway epithelium at 3 and 7 days post injury appears intact with no signs of injury   (MGI Ref ID J:167962)
      • after naphthalene administration to induce lung injury, the level of injury in the bronchial airway epithelium is reduced and repair is enhanced compared to controls   (MGI Ref ID J:167962)
  • respiratory system phenotype
  • abnormal lung morphology
    • lungs exhibit increased cell proliferation and decreased apoptosis   (MGI Ref ID J:167962)
    • lungs at 8 weeks of age sometimes contain a mass consisting of epithelial cells (putative progenitor cell masses) around the BADJ area; masses are slow growing and are organized into ductlike structures   (MGI Ref ID J:167962)
    • abnormal lung development
      • marker analysis indicates a block in transition from precursor to terminally differentiated cell types indicating impaired epithelial cell fate determination in the lung   (MGI Ref ID J:167962)
    • increased Clara cell number
      • increase in number of Clara cells in the lungs and a decrease in the number of ciliated cells, the terminally differentiated progeny of Clara cells   (MGI Ref ID J:167962)
    • pulmonary hyperplasia
      • progressive epithelial hyperplasia extending from the trachea to the small bronchioles is seen in the proximal lung epithelium from early stages of lung development and in adults   (MGI Ref ID J:167962)
  • increased lung endothelial cell proliferation
    • mutants exhibit an increase in the proliferation rate of the epithelial cells in E15.5 lungs   (MGI Ref ID J:167962)
    • expansion of epithelial cell populations occurs in multiple progenitor cell niches of the lungs including the tracheal basal cells in the proximal lung, the neuroepithelial bodies (NEB) in the distal bronchi and the progenitor cells occupying the bronchioalveolarduct junction (BADJ) region   (MGI Ref ID J:167962)
  • cellular phenotype
  • increased lung endothelial cell proliferation
    • mutants exhibit an increase in the proliferation rate of the epithelial cells in E15.5 lungs   (MGI Ref ID J:167962)
    • expansion of epithelial cell populations occurs in multiple progenitor cell niches of the lungs including the tracheal basal cells in the proximal lung, the neuroepithelial bodies (NEB) in the distal bronchi and the progenitor cells occupying the bronchioalveolarduct junction (BADJ) region   (MGI Ref ID J:167962)
  • endocrine/exocrine gland phenotype
  • abnormal thyroid gland morphology
    • at P14, epithelial cell proliferation rates in the thyroid are lower on the mixed BALB/c background than on the congenic C57BL/6 background at P14, epithelial cell proliferation rates in the thyroid are lower on the mixed BALB/c background than on the congenic C57BL/6 background   (MGI Ref ID J:197590)
    • at P14, thyroid architecture is conserved but an increase in the number of epithelial cells along the follicles is seen, resembling a goiter disease   (MGI Ref ID J:197590)
    • enlarged thyroid gland   (MGI Ref ID J:197590)
      • thyroid gland hyperplasia   (MGI Ref ID J:197590)
  • mortality/aging
  • *normal* mortality/aging
    • mutants survive to adulthood on the BALB/c background without presenting any obvious pathological conditions unlike mice on the congenic C57BL/6 background mutants survive to adulthood on the BALB/c background without presenting any obvious pathological conditions unlike mice on the congenic C57BL/6 background   (MGI Ref ID J:197590)

Ptentm1Hwu/Ptentm1Hwu Tg(Nkx2-1-cre)2Sand/0

        B6.Cg-Ptentm1Hwu Tg(Nkx2-1-cre)2Sand   (conditional)
  • endocrine/exocrine gland phenotype
  • abnormal thyroid gland morphology
    • at P14, thyroid architecture is altered, with multilayered epithelial cells surrounding the colloid lumen and with some dysmorphic follicles containing abnormal material inside   (MGI Ref ID J:197590)
    • abnormal thyroid follicle morphology
      • dysmorphic follicles containing abnormal material inside and multiple degenerative follicles which have varying degrees of colloid depletion are seen at P14   (MGI Ref ID J:197590)
    • enlarged thyroid gland
      • increase in thyroid size is already seen at E15.5 and is striking by P14   (MGI Ref ID J:197590)
      • thyroid gland hyperplasia
        • increase in epithelial cell proliferation rate at E15.5 and P14   (MGI Ref ID J:197590)
        • at P14, epithelial cell proliferation rates are higher on the congenic C57BL/6 background than on the BALB/c background   (MGI Ref ID J:197590)
  • homeostasis/metabolism phenotype
  • decreased thyroxine level
    • decrease in T4 hormonal levels at P14   (MGI Ref ID J:197590)
  • increased thyroid-stimulating hormone level
    • increase in TSH at P14   (MGI Ref ID J:197590)
  • mortality/aging
  • complete postnatal lethality
    • all mutants die before 2 weeks of age due to compression of the trachea and esophagus by the enlarged thyroid   (MGI Ref ID J:197590)
  • tumorigenesis
  • increased thyroid adenoma incidence
    • at P14, thyroid structure is completely altered with multiple degenerative follicles, which have varying degrees of colloid depletion, resembling a follicular adenoma   (MGI Ref ID J:197590)

Ptentm1Hwu/Ptentm1Hwu Tg(SFTPC-rtTA)5Jaw/0 Tg(tetO-cre)1Jaw/0

        involves: 129 * 129S4/SvJae * C57BL/6 * FVB/N   (conditional)
  • respiratory system phenotype
  • abnormal respiratory epithelium morphology
    • doxycyline treated mice exhibit an increase in proliferation of epithelial cells lining conducting airways   (MGI Ref ID J:146355)
    • abnormal lung epithelium morphology
      • papillary epithelial hyperplasia is seen as early as 4-6 weeks of age in mice treated with doxycycline   (MGI Ref ID J:146355)
      • papillary epithelial hyperplasia is characterized by a hypercellular epithelium lining papillae with fibrovascular cores that protrude into the airway lumens   (MGI Ref ID J:146355)
      • bronchial epithelial hyperplasia
        • mice treated with doxycycline exhibit bronchial epithelial hyperplasia, producing papillae composed of fibrovascular cores lined by a hypercellular epithelium protruding into the airway lumens consisting of enlarged cells   (MGI Ref ID J:146355)
      • bronchiolar epithelial hyperplasia
        • mice treated with doxycycline exhibit bronchiolar epithelial hyperplasia, producing papillae composed of fibrovascular cores lined by a hypercellular epithelium protruding into the airway lumens consisting of enlarged cells   (MGI Ref ID J:146355)
      • increased Clara cell number
        • doxycyline treated mice exhibit an increase in proliferation of nonciliated bronchial and bronchiolar Clara cells   (MGI Ref ID J:146355)
  • endocrine/exocrine gland phenotype
  • increased solitary pulmonary neuroendocrine cell number
    • pulmonary neuroepithelial cell hyperplasia, with a 2-fold increase in the number of pulmonary neuroendocrine cells in mice treated with doxycycline   (MGI Ref ID J:146355)
    • however normal respiratory epithelial cell differentiation and respiratory epithelial cell polarity   (MGI Ref ID J:146355)
  • nervous system phenotype
  • increased solitary pulmonary neuroendocrine cell number
    • pulmonary neuroepithelial cell hyperplasia, with a 2-fold increase in the number of pulmonary neuroendocrine cells in mice treated with doxycycline   (MGI Ref ID J:146355)
    • however normal respiratory epithelial cell differentiation and respiratory epithelial cell polarity   (MGI Ref ID J:146355)
  • tumorigenesis
  • *normal* tumorigenesis
    • overt pulmonary tumors are not observed in doxycycline treated mice at 6 weeks of age   (MGI Ref ID J:146355)

Ptentm1Hwu/Ptentm1Hwu Tg(Vil-cre)997Gum/0

        involves: 129S4/SvJae * BALB/c * C57BL/6J * SJL   (conditional)
  • digestive/alimentary phenotype
  • abnormal intestine morphology
    • intestine is 1.28-fold longer and weighs 1.58-fold more than controls   (MGI Ref ID J:150553)
    • however, mutants do not develop polyps   (MGI Ref ID J:150553)
    • abnormal intestinal mucosa morphology
      • thickening of the intestinal mucosa   (MGI Ref ID J:150553)
      • abnormal intestinal enteroendocrine cell morphology
        • decrease in the number of enteroendocrine cells   (MGI Ref ID J:150553)
      • abnormal intestinal goblet cell morphology
        • increase in the number and size of goblet cells   (MGI Ref ID J:150553)
      • abnormal small intestine crypts of Lieberkuhn morphology
        • small intestine exhibits an expanded crypt compartment with increased number of crypts per villus   (MGI Ref ID J:150553)
        • abnormal Paneth cell morphology
          • marker analysis indicates impaired Paneth cell maturation   (MGI Ref ID J:150553)
    • abnormal small intestine morphology
      • thickening of the muscular layers of the small intestine   (MGI Ref ID J:150553)
      • abnormal duodenum morphology
        • total protein content of the duodenum is enhanced by 50%   (MGI Ref ID J:150553)
      • abnormal jejunum morphology
        • jejunum exhibits expanded crypt and villus compartments, an increased number of crypts, thickening of the muscular layers and villus branching   (MGI Ref ID J:150553)
      • abnormal small intestinal villus morphology
        • small intestine exhibits an expanded villus compartment   (MGI Ref ID J:150553)
        • mutants exhibit branching of the villi in the small intestine   (MGI Ref ID J:150553)
      • abnormal small intestine crypts of Lieberkuhn morphology
        • small intestine exhibits an expanded crypt compartment with increased number of crypts per villus   (MGI Ref ID J:150553)
        • abnormal Paneth cell morphology
          • marker analysis indicates impaired Paneth cell maturation   (MGI Ref ID J:150553)
  • abnormal small intestinal crypt cell proliferation
    • increase in crypt cell proliferation   (MGI Ref ID J:150553)
  • endocrine/exocrine gland phenotype
  • abnormal small intestine crypts of Lieberkuhn morphology
    • small intestine exhibits an expanded crypt compartment with increased number of crypts per villus   (MGI Ref ID J:150553)
    • abnormal Paneth cell morphology
      • marker analysis indicates impaired Paneth cell maturation   (MGI Ref ID J:150553)
  • cellular phenotype
  • abnormal small intestinal crypt cell proliferation
    • increase in crypt cell proliferation   (MGI Ref ID J:150553)

Ptentm1Hwu/Ptentm1Hwu Tg(Zp3-cre)93Knw/0

        B6.Cg-Ptentm1Hwu Tg(Zp3-cre)93Knw   (conditional)
  • reproductive system phenotype
  • *normal* reproductive system phenotype
    • mice exhibit normal follicular development, showing healthy corpora lutea and preovulatory follicles at 16 weeks of age, normal resumption of meiosis, ovulation, fertilization and fertility, although PI3K-Akt signaling is elevated   (MGI Ref ID J:151696)

Ptentm1Hwu/Ptentm1Hwu Slc6a3tm1.1(cre)Bkmn/Slc6a3+

        involves: 129S4/SvJae * C57BL/6   (conditional)
  • behavior/neurological phenotype
  • *normal* behavior/neurological phenotype
    • no difference in locomotor activity is seen compared to controls during exposure to a novel environment   (MGI Ref ID J:153622)
    • abnormal behavioral response to xenobiotic
      • mutants exhibit a significant reduction in ipsilateral rotational behavior in response to amphetamine administration after 6OHDA lesioning   (MGI Ref ID J:153622)
  • nervous system phenotype
  • abnormal dopaminergic neuron morphology
    • increase in number of dopaminergic neurons and fibers in the ventral mesencephalon   (MGI Ref ID J:153622)
    • dopaminergic neurons in the ventral midbrain are larger in size and have an increase in the number of dendritic processes in the substantia nigra pars reticulata   (MGI Ref ID J:153622)
  • abnormal midbrain morphology
    • neuronal hypertrophy in the ventral midbrain resulting in enlargement of the ventral midbrain area   (MGI Ref ID J:153622)
    • increase in the number of TH positive neurons in the substantia nigra compacta and ventral tegmental area of the adult ventral midbrain and an increase in neuronal soma size   (MGI Ref ID J:153622)
    • abnormal substantia nigra pars compacta morphology
      • increase in the number of TH positive neurons in the substantia nigra compacta   (MGI Ref ID J:153622)
    • abnormal substantia nigra pars reticulata morphology
      • increase in the number of dopaminergic neuron dendritic processes in the substantia nigra pars reticulata   (MGI Ref ID J:153622)
  • abnormal nervous system physiology
    • mutant dopamine neurons are protected from 6OHDA induced lesions, fiber loss, and axonal loss in the striatum compared to controls   (MGI Ref ID J:153622)
    • increased dopamine level
      • increase in total dopamine tissue levels in the dorsal striatum and midbrain, however, no alterations in basal dopamine extracellular levels or evoked dopamine release in the dorsal striatum   (MGI Ref ID J:153622)
  • abnormal striatum morphology
    • modest but significant enlargement of the caudal striatum   (MGI Ref ID J:153622)
  • neuron hypertrophy
    • hypertrophy of dopamine neurons   (MGI Ref ID J:153622)
  • homeostasis/metabolism phenotype
  • increased dopamine level
    • increase in total dopamine tissue levels in the dorsal striatum and midbrain, however, no alterations in basal dopamine extracellular levels or evoked dopamine release in the dorsal striatum   (MGI Ref ID J:153622)

Ptentm1Hwu/Ptentm1Hwu Twist2tm1.1(cre)Dor/Twist2+

        B6.129-Twist2tm1.1(cre)Dor Ptentm1Hwu   (conditional)
  • mortality/aging
  • complete neonatal lethality
    • mutants with less severe phenotypes die within 2-3 hours of birth, displaying cyanosis, chest retractions, and dyspnea   (MGI Ref ID J:192736)
  • partial lethality throughout fetal growth and development
    • lethality between E15.5 and E18.5   (MGI Ref ID J:192736)
  • respiratory system phenotype
  • abnormal lung morphology
    • increase in collagen deposition in the lungs   (MGI Ref ID J:192736)
    • alveolar spaces are frequently lined by cuboidal cells with immature lamellar bodies   (MGI Ref ID J:192736)
    • abnormal lung development
      • marker analysis indicates expansion of the distal epithelial progenitor cell domain   (MGI Ref ID J:192736)
      • abnormal lung-associated mesenchyme development
        • E18.5 lungs exhibit a hypercellular mesenchymal compartment   (MGI Ref ID J:192736)
        • more than 5-fold increase in the number of CD45-CD31+ embryonic mesenchymal progenitor side population (E-SP) and CD45-CD31- E-SP cell populations in E17.5 lungs indicating an increase in lung mesenchymal progenitor cell populations   (MGI Ref ID J:192736)
    • abnormal lung vasculature morphology
      • reduction in distal capillary network density in E15.5 lungs   (MGI Ref ID J:192736)
      • the capillary network is misaligned with corresponding respiratory airways (airway/capillary uncoupling or dysplasia) at E18.5   (MGI Ref ID J:192736)
      • increase in the distance between the capillaries and the lumen of the airways   (MGI Ref ID J:192736)
  • respiratory distress
    • in mutants with less severe phenotypes that die within hours of birth   (MGI Ref ID J:192736)
  • cardiovascular system phenotype
  • abnormal lung vasculature morphology
    • reduction in distal capillary network density in E15.5 lungs   (MGI Ref ID J:192736)
    • the capillary network is misaligned with corresponding respiratory airways (airway/capillary uncoupling or dysplasia) at E18.5   (MGI Ref ID J:192736)
    • increase in the distance between the capillaries and the lumen of the airways   (MGI Ref ID J:192736)
  • abnormal vascular development
    • 44% of embryos lack of vascularization in entire embryos at E15.5   (MGI Ref ID J:192736)
    • E15.5 embryos show lack of vascularization in organs such as limbs and liver   (MGI Ref ID J:192736)
    • impaired differentiation of angioblasts into mature endothelial cells and blood vessels   (MGI Ref ID J:192736)
  • hemorrhage
    • 15% of embryos exhibit hemorrhage at E18.5   (MGI Ref ID J:192736)
  • homeostasis/metabolism phenotype
  • cyanosis
    • in mutants with less severe phenotypes that die within hours of birth   (MGI Ref ID J:192736)
  • decreased blood oxygen capacity
    • newborns show a decrease in blood oxygenation   (MGI Ref ID J:192736)
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Ptentm1Hwu related

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Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Ptentm1Hwu
Allele Name targeted mutation 1, Hong Wu
Allele Type Targeted (Conditional ready (e.g. floxed), No functional change)
Common Name(s) PTENF; Ptenex5lox; Ptenfl; Ptenflox; Ptenfx; Ptenlox; Ptenloxp;
Mutation Made By Hong Wu,   UCLA
Strain of Origin129S4/SvJae
ES Cell Line NameLW1
ES Cell Line Strain129S4/SvJae
Site of ExpressionPten is a widely expressed tumor suppresser gene.
Gene Symbol and Name Pten, phosphatase and tensin homolog
Chromosome 19
Gene Common Name(s) 10q23del; 2310035O07Rik; A130070J02Rik; AI463227; B430203M17Rik; BZS; CWS1; DEC; GLM2; MHAM; MMAC1; Mmac; PTEN1; RIKEN cDNA 2310035O07 gene; RIKEN cDNA A130070J02 gene; RIKEN cDNA B430203M17 gene; TEP1; expressed sequence AI463227;
General Note Phenotypic Similarity to Human Syndrome: Chronic intestinal pseudoobstruction J:155110.

Phenotypic Similarity to Human Syndrome: Granulosa cell tumor of the testis (GCTT) J:149060.

Phenotypic Similarity to Human Syndrome: Granulosa cell tumor (GCT) J:142150.

Phenotypic Similarity to Human Syndrome: Glioblastoma J:172585.

Phenotypic Similarity to Human Syndrome: B cell lymphoma J:166155.

Phenotypic Similarity to Human Syndrome: Astrocytoma J:134611

Phenotypic Similarity to Human Syndrome: Thyroid Carcinoma (J:177181)

Phenotypic Similarity to Human Syndrome: Granulosa cell tumor (GCT) J:186144

Phenotypic Similarity to Human Syndrome: Granulosa cell tumor of the testis (GCTT) J:186144

Phenotypic Similarity to Human Syndrome: PTEN Hamartoma Tumor Syndrome (see OMIM:601728 Phosphatase And Tensin Homolog; PTEN) J:199362

Molecular Note A loxP flanked hygromycin resistance cassette was inserted 5' to exon 5, and a single loxP site was inserted 3' to exon 5, which encodes the phosphatase domain. The hygromycin cassette was removed in ES cells by transient Cre recombinase expression prior to the production of chimeric mice, leaving a single loxP site in place of the cassette. These insertions do not appear to have any effect on the normal function of the gene. [MGI Ref ID J:75117]

Genotyping

Genotyping Information

Genotyping Protocols

Ptentm1Hwu, Melt Curve Analysis
Ptentm1Hwu, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Lesche R; Groszer M; Gao J; Wang Y; Messing A; Sun H; Liu X; Wu H. 2002. Cre/loxP-mediated inactivation of the murine Pten tumor suppressor gene. Genesis 32(2):148-9. [PubMed: 11857804]  [MGI Ref ID J:75117]

Additional References

Ptentm1Hwu related

Adhikari D; Zheng W; Shen Y; Gorre N; Hamalainen T; Cooney AJ; Huhtaniemi I; Lan ZJ; Liu K. 2009. Tsc/mTORC1 signaling in oocytes governs the quiescence and activation of primordial follicles. Hum Mol Genet :. [PubMed: 19843540]  [MGI Ref ID J:155357]

Adisetiyo H; Liang M; Liao CP; Aycock-Williams A; Cohen MB; Xu S; Neamati N; Conway EM; Cheng CY; Nikitin AY; Roy-Burman P. 2013. Loss of survivin in the prostate epithelium impedes carcinogenesis in a mouse model of prostate adenocarcinoma. PLoS One 8(7):e69484. [PubMed: 23936028]  [MGI Ref ID J:203267]

Ahmad I; Morton JP; Singh LB; Radulescu SM; Ridgway RA; Patel S; Woodgett J; Winton DJ; Taketo MM; Wu XR; Leung HY; Sansom OJ. 2010. beta-Catenin activation synergizes with PTEN loss to cause bladder cancer formation. Oncogene :. [PubMed: 20818428]  [MGI Ref ID J:164579]

Ahmad I; Patel R; Singh LB; Nixon C; Seywright M; Barnetson RJ; Brunton VG; Muller WJ; Edwards J; Sansom OJ; Leung HY. 2011. HER2 overcomes PTEN (loss)-induced senescence to cause aggressive prostate cancer. Proc Natl Acad Sci U S A 108(39):16392-7. [PubMed: 21930937]  [MGI Ref ID J:177138]

Ahmad I; Singh LB; Foth M; Morris CA; Taketo MM; Wu XR; Leung HY; Sansom OJ; Iwata T. 2011. K-Ras and {beta}-catenin mutations cooperate with Fgfr3 mutations in mice to promote tumorigenesis in the skin and lung, but not in the bladder. Dis Model Mech 4(4):548-55. [PubMed: 21504907]  [MGI Ref ID J:174242]

Akins EJ; Moore ML; Tang S; Willingham MC; Tooze JA; Dubey P. 2010. In situ vaccination combined with androgen ablation and regulatory T-cell depletion reduces castration-resistant tumor burden in prostate-specific pten knockout mice. Cancer Res 70(9):3473-82. [PubMed: 20406970]  [MGI Ref ID J:159457]

Alcantara Llaguno S; Chen J; Kwon CH; Jackson EL; Li Y; Burns DK; Alvarez-Buylla A; Parada LF. 2009. Malignant astrocytomas originate from neural stem/progenitor cells in a somatic tumor suppressor mouse model. Cancer Cell 15(1):45-56. [PubMed: 19111880]  [MGI Ref ID J:143505]

Anzelon AN; Wu H; Rickert RC. 2003. Pten inactivation alters peripheral B lymphocyte fate and reconstitutes CD19 function. Nat Immunol 4(3):287-94. [PubMed: 12563260]  [MGI Ref ID J:83213]

Aytes A; Mitrofanova A; Kinkade CW; Lefebvre C; Lei M; Phelan V; Lekaye HC; Koutcher JA; Cardiff RD; Califano A; Shen MM; Abate-Shen C. 2013. ETV4 promotes metastasis in response to activation of PI3-kinase and Ras signaling in a mouse model of advanced prostate cancer. Proc Natl Acad Sci U S A 110(37):E3506-15. [PubMed: 23918374]  [MGI Ref ID J:200917]

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Srinivasan L; Sasaki Y; Calado DP; Zhang B; Paik JH; DePinho RA; Kutok JL; Kearney JF; Otipoby KL; Rajewsky K. 2009. PI3 kinase signals BCR-dependent mature B cell survival. Cell 139(3):573-86. [PubMed: 19879843]  [MGI Ref ID J:157297]

Stanger BZ; Stiles B; Lauwers GY; Bardeesy N; Mendoza M; Wang Y; Greenwood A; Cheng KH; McLaughlin M; Brown D; Depinho RA; Wu H; Melton DA; Dor Y. 2005. Pten constrains centroacinar cell expansion and malignant transformation in the pancreas. Cancer Cell 8(3):185-95. [PubMed: 16169464]  [MGI Ref ID J:102226]

Stiles B; Wang Y; Stahl A; Bassilian S; Lee WP; Kim YJ; Sherwin R; Devaskar S; Lesche R; Magnuson MA; Wu H. 2004. Liver-specific deletion of negative regulator Pten results in fatty liver and insulin hypersensitivity [corrected]. Proc Natl Acad Sci U S A 101(7):2082-7. [PubMed: 14769918]  [MGI Ref ID J:88441]

Stiles BL; Kuralwalla-Martinez C; Guo W; Gregorian C; Wang Y; Tian J; Magnuson MA; Wu H. 2006. Selective deletion of Pten in pancreatic beta cells leads to increased islet mass and resistance to STZ-induced diabetes. Mol Cell Biol 26(7):2772-81. [PubMed: 16537919]  [MGI Ref ID J:106937]

Subramanian KK; Jia Y; Zhu D; Simms BT; Jo H; Hattori H; You J; Mizgerd JP; Luo HR. 2007. Tumor suppressor PTEN is a physiologic suppressor of chemoattractant-mediated neutrophil functions. Blood 109(9):4028-37. [PubMed: 17202315]  [MGI Ref ID J:145331]

Sun C; Zhao J; Jin Y; Hou C; Zong W; Lu T; Li H; Gao J. 2014. PTEN regulation of the proliferation and differentiation of auditory progenitors through the PTEN/PI3K/Akt-signaling pathway in mice. Neuroreport 25(3):177-83. [PubMed: 24481416]  [MGI Ref ID J:206951]

Sun X; Jackson L; Dey SK; Daikoku T. 2009. In pursuit of leucine-rich repeat-containing G protein-coupled receptor-5 regulation and function in the uterus. Endocrinology 150(11):5065-73. [PubMed: 19797400]  [MGI Ref ID J:157315]

Sun ZJ; Zhang L; Hall B; Bian Y; Gutkind JS; Kulkarni AB. 2012. Chemopreventive and chemotherapeutic actions of mTOR inhibitor in genetically defined head and neck squamous cell carcinoma mouse model. Clin Cancer Res 18(19):5304-13. [PubMed: 22859719]  [MGI Ref ID J:194652]

Svensson RU; Haverkamp JM; Thedens DR; Cohen MB; Ratliff TL; Henry MD. 2011. Slow disease progression in a C57BL/6 pten-deficient mouse model of prostate cancer. Am J Pathol 179(1):502-12. [PubMed: 21703427]  [MGI Ref ID J:173997]

Tandon P; Gallo CA; Khatri S; Barger JF; Yepiskoposyan H; Plas DR. 2011. Requirement for ribosomal protein S6 kinase 1 to mediate glycolysis and apoptosis resistance induced by Pten deficiency. Proc Natl Acad Sci U S A 108(6):2361-5. [PubMed: 21262837]  [MGI Ref ID J:169097]

Tang S; Moore ML; Grayson JM; Dubey P. 2012. Increased CD8+ T-cell function following castration and immunization is countered by parallel expansion of regulatory T cells. Cancer Res 72(8):1975-85. [PubMed: 22374980]  [MGI Ref ID J:185631]

Tanwar PS; Commandeur AE; Zhang L; Taketo MM; Teixeira JM. 2012. The Mullerian inhibiting substance type 2 receptor suppresses tumorigenesis in testes with sustained beta-catenin signaling. Carcinogenesis 33(12):2351-61. [PubMed: 22962306]  [MGI Ref ID J:193300]

Tanwar PS; Kaneko-Tarui T; Zhang L; Tanaka Y; Crum CP; Teixeira JM. 2012. Stromal liver kinase B1 [STK11] signaling loss induces oviductal adenomas and endometrial cancer by activating mammalian Target of Rapamycin Complex 1. PLoS Genet 8(8):e1002906. [PubMed: 22916036]  [MGI Ref ID J:188124]

Tanwar PS; Kaneko-Tarui T; Zhang L; Teixeira JM. 2012. Altered LKB1/AMPK/TSC1/TSC2/mTOR signaling causes disruption of Sertoli cell polarity and spermatogenesis. Hum Mol Genet 21(20):4394-405. [PubMed: 22791749]  [MGI Ref ID J:187754]

Tanwar PS; Mohapatra G; Chiang S; Engler DA; Zhang L; Kaneko-Tarui T; Ohguchi Y; Birrer MJ; Teixeira JM. 2014. Loss of LKB1 and PTEN tumor suppressor genes in the ovarian surface epithelium induces papillary serous ovarian cancer. Carcinogenesis 35(3):546-53. [PubMed: 24170201]  [MGI Ref ID J:206514]

Tanwar PS; Zhang L; Kaneko-Tarui T; Curley MD; Taketo MM; Rani P; Roberts DJ; Teixeira JM. 2011. Mammalian Target of Rapamycin Is a Therapeutic Target for Murine Ovarian Endometrioid Adenocarcinomas with Dysregulated Wnt/beta-Catenin and PTEN. PLoS One 6(6):e20715. [PubMed: 21695255]  [MGI Ref ID J:174289]

Tesio M; Oser GM; Baccelli I; Blanco-Bose W; Wu H; Gothert JR; Kogan SC; Trumpp A. 2013. Pten loss in the bone marrow leads to G-CSF-mediated HSC mobilization. J Exp Med 210(11):2337-49. [PubMed: 24127490]  [MGI Ref ID J:206536]

Thomsen MK; Ambroisine L; Wynn S; Cheah KS; Foster CS; Fisher G; Berney DM; Moller H; Reuter VE; Scardino P; Cuzick J; Ragavan N; Singh PB; Martin FL; Butler CM; Cooper CS; Swain A. 2010. SOX9 elevation in the prostate promotes proliferation and cooperates with PTEN loss to drive tumor formation. Cancer Res 70(3):979-87. [PubMed: 20103652]  [MGI Ref ID J:156856]

Tien JC; Liu Z; Liao L; Wang F; Xu Y; Wu YL; Zhou N; Ittmann M; Xu J. 2013. The steroid receptor coactivator-3 is required for the development of castration-resistant prostate cancer. Cancer Res 73(13):3997-4008. [PubMed: 23650284]  [MGI Ref ID J:199012]

Ting MC; Liao CP; Yan C; Jia L; Groshen S; Frenkel B; Roy-Burman P; Coetzee GA; Maxson R. 2012. An enhancer from the 8q24 prostate cancer risk region is sufficient to direct reporter gene expression to a subset of prostate stem-like epithelial cells in transgenic mice. Dis Model Mech 5(3):366-74. [PubMed: 22279083]  [MGI Ref ID J:181487]

Tiozzo C; Carraro G; Al Alam D; Baptista S; Danopoulos S; Li A; Lavarreda-Pearce M; Li C; De Langhe S; Chan B; Borok Z; Bellusci S; Minoo P. 2012. Mesodermal Pten inactivation leads to alveolar capillary dysplasia- like phenotype. J Clin Invest 122(11):3862-72. [PubMed: 23023706]  [MGI Ref ID J:192736]

Tiozzo C; Danopoulos S; Lavarreda-Pearce M; Baptista S; Varimezova R; Al Alam D; Warburton D; Rehan V; De Langhe S; Di Cristofano A; Bellusci S; Minoo P. 2012. Embryonic epithelial Pten deletion through Nkx2.1-cre leads to thyroid tumorigenesis in a strain-dependent manner. Endocr Relat Cancer 19(2):111-22. [PubMed: 22167068]  [MGI Ref ID J:197590]

Tiozzo C; De Langhe S; Yu M; Londhe VA; Carraro G; Li M; Li C; Xing Y; Anderson S; Borok Z; Bellusci S; Minoo P. 2009. Deletion of Pten expands lung epithelial progenitor pools and confers resistance to airway injury. Am J Respir Crit Care Med 180(8):701-12. [PubMed: 19574443]  [MGI Ref ID J:167962]

Vitari AC; Leong KG; Newton K; Yee C; O'Rourke K; Liu J; Phu L; Vij R; Ferrando R; Couto SS; Mohan S; Pandita A; Hongo JA; Arnott D; Wertz IE; Gao WQ; French DM; Dixit VM. 2011. COP1 is a tumour suppressor that causes degradation of ETS transcription factors. Nature 474(7351):403-6. [PubMed: 21572435]  [MGI Ref ID J:172653]

Vivanco I; Rohle D; Versele M; Iwanami A; Kuga D; Oldrini B; Tanaka K; Dang J; Kubek S; Palaskas N; Hsueh T; Evans M; Mulholland D; Wolle D; Rajasekaran S; Rajasekaran A; Liau LM; Cloughesy TF; Dikic I; Brennan C; Wu H; Mischel PS; Perera T; Mellinghoff IK. 2010. The phosphatase and tensin homolog regulates epidermal growth factor receptor (EGFR) inhibitor response by targeting EGFR for degradation. Proc Natl Acad Sci U S A 107(14):6459-64. [PubMed: 20308550]  [MGI Ref ID J:159321]

Wang J; Kobayashi T; Floc'h N; Kinkade CW; Aytes A; Dankort D; Lefebvre C; Mitrofanova A; Cardiff RD; McMahon M; Califano A; Shen MM; Abate-Shen C. 2012. B-Raf activation cooperates with PTEN loss to drive c-Myc expression in advanced prostate cancer. Cancer Res 72(18):4765-76. [PubMed: 22836754]  [MGI Ref ID J:191327]

Wang L; Liu Y; Yan Lu S; Nguyen KT; Schroer SA; Suzuki A; Mak TW; Gaisano H; Woo M. 2010. Deletion of Pten in pancreatic ss-cells protects against deficient ss-cell mass and function in mouse models of type 2 diabetes. Diabetes 59(12):3117-26. [PubMed: 20852026]  [MGI Ref ID J:170206]

Wang Q; Li SH; Wang H; Xiao Y; Sahin O; Brady SW; Li P; Ge H; Jaffee EM; Muller WJ; Hortobagyi GN; Yu D. 2012. Concomitant targeting of tumor cells and induction of T-cell response synergizes to effectively inhibit trastuzumab-resistant breast cancer. Cancer Res 72(17):4417-28. [PubMed: 22773664]  [MGI Ref ID J:191018]

Wang Q; Von T; Bronson R; Ruan M; Mu W; Huang A; Maira SM; Zhao JJ. 2013. Spatially distinct roles of class Ia PI3K isoforms in the development and maintenance of PTEN hamartoma tumor syndrome. Genes Dev 27(14):1568-80. [PubMed: 23873941]  [MGI Ref ID J:199362]

Wang S; Gao J; Lei Q; Rozengurt N; Pritchard C; Jiao J; Thomas GV; Li G; Roy-Burman P; Nelson PS; Liu X; Wu H. 2003. Prostate-specific deletion of the murine Pten tumor suppressor gene leads to metastatic prostate cancer. Cancer Cell 4(3):209-21. [PubMed: 14522255]  [MGI Ref ID J:93902]

Wang S; Garcia AJ; Wu M; Lawson DA; Witte ON; Wu H. 2006. Pten deletion leads to the expansion of a prostatic stem/progenitor cell subpopulation and tumor initiation. Proc Natl Acad Sci U S A 103(5):1480-5. [PubMed: 16432235]  [MGI Ref ID J:105995]

Wang S; Wu J; Suburu J; Gu Z; Cai J; Axanova LS; Cramer SD; Thomas MJ; Perry DL; Edwards IJ; Mucci LA; Sinnott JA; Loda MF; Sui G; Berquin IM; Chen YQ. 2012. Effect of dietary polyunsaturated fatty acids on castration-resistant Pten-null prostate cancer. Carcinogenesis 33(2):404-12. [PubMed: 22159221]  [MGI Ref ID J:181111]

Wang X; Kruithof-de Julio M; Economides KD; Walker D; Yu H; Halili MV; Hu YP; Price SM; Abate-Shen C; Shen MM. 2009. A luminal epithelial stem cell that is a cell of origin for prostate cancer. Nature 461(7263):495-500. [PubMed: 19741607]  [MGI Ref ID J:153425]

Wang ZA; Mitrofanova A; Bergren SK; Abate-Shen C; Cardiff RD; Califano A; Shen MM. 2013. Lineage analysis of basal epithelial cells reveals their unexpected plasticity and supports a cell-of-origin model for prostate cancer heterogeneity. Nat Cell Biol 15(3):274-83. [PubMed: 23434823]  [MGI Ref ID J:195200]

Weng Z; Li D; Zhang L; Chen J; Ruan C; Chen G; Gartner TK; Liu J. 2010. PTEN regulates collagen-induced platelet activation. Blood 116(14):2579-81. [PubMed: 20554973]  [MGI Ref ID J:165893]

Wey S; Luo B; Tseng CC; Ni M; Zhou H; Fu Y; Bhojwani D; Carroll WL; Lee AS. 2012. Inducible knockout of GRP78/BiP in the hematopoietic system suppresses Pten-null leukemogenesis and AKT oncogenic signaling. Blood 119(3):817-25. [PubMed: 21937694]  [MGI Ref ID J:181587]

White AC; Khuu JK; Dang CY; Hu J; Tran KV; Liu A; Gomez S; Zhang Z; Yi R; Scumpia P; Grigorian M; Lowry WE. 2014. Stem cell quiescence acts as a tumour suppressor in squamous tumours. Nat Cell Biol 16(1):99-107. [PubMed: 24335650]  [MGI Ref ID J:208368]

Woolfenden S; Zhu H; Charest A. 2009. A Cre/LoxP conditional luciferase reporter transgenic mouse for bioluminescence monitoring of tumorigenesis. Genesis 47(10):659-666. [PubMed: 19603508]  [MGI Ref ID J:153565]

Xiao C; Srinivasan L; Calado DP; Patterson HC; Zhang B; Wang J; Henderson JM; Kutok JL; Rajewsky K. 2008. Lymphoproliferative disease and autoimmunity in mice with increased miR-17-92 expression in lymphocytes. Nat Immunol 9(4):405-14. [PubMed: 18327259]  [MGI Ref ID J:133215]

Xing Y; Li C; Hu L; Tiozzo C; Li M; Chai Y; Bellusci S; Anderson S; Minoo P. 2008. Mechanisms of TGFbeta inhibition of LUNG endodermal morphogenesis: the role of TbetaRII, Smads, Nkx2.1 and Pten. Dev Biol 320(2):340-50. [PubMed: 18602626]  [MGI Ref ID J:138200]

Xing Y; Li C; Li A; Sridurongrit S; Tiozzo C; Bellusci S; Borok Z; Kaartinen V; Minoo P. 2010. Signaling via Alk5 controls the ontogeny of lung Clara cells. Development 137(5):825-33. [PubMed: 20147383]  [MGI Ref ID J:157922]

Xu X; Ehdaie B; Ohara N; Yoshino T; Deng CX. 2010. Synergistic action of Smad4 and Pten in suppressing pancreatic ductal adenocarcinoma formation in mice. Oncogene 29(5):674-86. [PubMed: 19901970]  [MGI Ref ID J:157020]

Xu X; Kobayashi S; Qiao W; Li C; Xiao C; Radaeva S; Stiles B; Wang RH; Ohara N; Yoshino T; LeRoith D; Torbenson MS; Gores GJ; Wu H; Gao B; Deng CX. 2006. Induction of intrahepatic cholangiocellular carcinoma by liver-specific disruption of Smad4 and Pten in mice. J Clin Invest 116(7):1843-52. [PubMed: 16767220]  [MGI Ref ID J:111718]

Yang Y; Iwanaga K; Raso MG; Wislez M; Hanna AE; Wieder ED; Molldrem JJ; Wistuba II; Powis G; Demayo FJ; Kim CF; Kurie JM. 2008. Phosphatidylinositol 3-kinase mediates bronchioalveolar stem cell expansion in mouse models of oncogenic K-ras-induced lung cancer. PLoS ONE 3(5):e2220. [PubMed: 18493606]  [MGI Ref ID J:136369]

Yang ZF; Zhang H; Ma L; Peng C; Chen Y; Wang J; Green MR; Li S; Rosmarin AG. 2013. GABP transcription factor is required for development of chronic myelogenous leukemia via its control of PRKD2. Proc Natl Acad Sci U S A 110(6):2312-7. [PubMed: 23345428]  [MGI Ref ID J:194335]

Yao D; Alexander CL; Quinn JA; Chan WC; Wu H; Greenhalgh DA. 2008. Fos cooperation with PTEN loss elicits keratoacanthoma not carcinoma, owing to p53/p21 WAF-induced differentiation triggered by GSK3beta inactivation and reduced AKT activity. J Cell Sci 121(Pt 10):1758-69. [PubMed: 18445683]  [MGI Ref ID J:138532]

Yao D; Alexander CL; Quinn JA; Porter MJ; Wu H; Greenhalgh DA. 2006. PTEN loss promotes rasHa-mediated papillomatogenesis via dual up-regulation of AKT activity and cell cycle deregulation but malignant conversion proceeds via PTEN-associated pathways. Cancer Res 66(3):1302-12. [PubMed: 16452183]  [MGI Ref ID J:106683]

Yeh ES; Belka GK; Vernon AE; Chen CC; Jung JJ; Chodosh LA. 2013. Hunk negatively regulates c-myc to promote Akt-mediated cell survival and mammary tumorigenesis induced by loss of Pten. Proc Natl Acad Sci U S A 110(15):6103-8. [PubMed: 23520049]  [MGI Ref ID J:196198]

Yilmaz OH; Valdez R; Theisen BK; Guo W; Ferguson DO; Wu H; Morrison SJ. 2006. Pten dependence distinguishes haematopoietic stem cells from leukaemia-initiating cells. Nature 441(7092):475-82. [PubMed: 16598206]  [MGI Ref ID J:109085]

Yoo LI; Liu DW; Le Vu S; Bronson RT; Wu H; Yuan J. 2006. Pten deficiency activates distinct downstream signaling pathways in a tissue-specific manner. Cancer Res 66(4):1929-39. [PubMed: 16488991]  [MGI Ref ID J:106662]

Yoshioka T; Otero J; Chen Y; Kim YM; Koutcher JA; Satagopan J; Reuter V; Carver B; de Stanchina E; Enomoto K; Greenberg NM; Scardino PT; Scher HI; Sawyers CL; Giancotti FG. 2013. beta4 Integrin signaling induces expansion of prostate tumor progenitors. J Clin Invest :. [PubMed: 23348745]  [MGI Ref ID J:194482]

Yue Q; Groszer M; Gil JS; Berk AJ; Messing A; Wu H; Liu X. 2005. PTEN deletion in Bergmann glia leads to premature differentiation and affects laminar organization. Development 132(14):3281-91. [PubMed: 15944184]  [MGI Ref ID J:100428]

Zeiser R; Leveson-Gower DB; Zambricki EA; Kambham N; Beilhack A; Loh J; Hou JZ; Negrin RS. 2008. Differential impact of mammalian target of rapamycin inhibition on CD4+CD25+Foxp3+ regulatory T cells compared with conventional CD4+ T cells. Blood 111(1):453-62. [PubMed: 17967941]  [MGI Ref ID J:130295]

Zhang J; Grindley JC; Yin T; Jayasinghe S; He XC; Ross JT; Haug JS; Rupp D; Porter-Westpfahl KS; Wiedemann LM; Wu H; Li L. 2006. PTEN maintains haematopoietic stem cells and acts in lineage choice and leukaemia prevention. Nature 441(7092):518-22. [PubMed: 16633340]  [MGI Ref ID J:109084]

Zhang L; Sun ZJ; Bian Y; Kulkarni AB. 2013. MicroRNA-135b acts as a tumor promoter by targeting the hypoxia-inducible factor pathway in genetically defined mouse model of head and neck squamous cell carcinoma. Cancer Lett 331(2):230-8. [PubMed: 23340180]  [MGI Ref ID J:194341]

Zhang Q; Liu S; Ge D; Zhang Q; Xue Y; Xiong Z; Abdel-Mageed AB; Myers L; Hill SM; Rowan BG; Sartor O; Melamed J; Chen Z; You Z. 2012. Interleukin-17 promotes formation and growth of prostate adenocarcinoma in mouse models. Cancer Res 72(10):2589-99. [PubMed: 22461511]  [MGI Ref ID J:189341]

Zhang W; Zhu J; Efferson CL; Ware C; Tammam J; Angagaw M; Laskey J; Bettano KA; Kasibhatla S; Reilly JF; Sur C; Majumder PK. 2009. Inhibition of tumor growth progression by antiandrogens and mTOR inhibitor in a Pten-deficient mouse model of prostate cancer. Cancer Res 69(18):7466-72. [PubMed: 19738074]  [MGI Ref ID J:152681]

Zheng W; Gorre N; Shen Y; Noda T; Ogawa W; Lundin E; Liu K. 2010. Maternal phosphatidylinositol 3-kinase signalling is crucial for embryonic genome activation and preimplantation embryogenesis. EMBO Rep 11(11):890-5. [PubMed: 20930845]  [MGI Ref ID J:165798]

Zhong C; Saribekyan G; Liao CP; Cohen MB; Roy-Burman P. 2006. Cooperation between FGF8b overexpression and PTEN deficiency in prostate tumorigenesis. Cancer Res 66(4):2188-94. [PubMed: 16489020]  [MGI Ref ID J:106650]

Zhong J; Ding L; Bohrer LR; Pan Y; Liu P; Zhang J; Sebo TJ; Karnes RJ; Tindall DJ; van Deursen J; Huang H. 2014. p300 acetyltransferase regulates androgen receptor degradation and PTEN-deficient prostate tumorigenesis. Cancer Res 74(6):1870-80. [PubMed: 24480624]  [MGI Ref ID J:208327]

Zhu D; Hattori H; Jo H; Jia Y; Subramanian KK; Loison F; You J; Le Y; Honczarenko M; Silberstein L; Luo HR. 2006. Deactivation of phosphatidylinositol 3,4,5-trisphosphate/Akt signaling mediates neutrophil spontaneous death. Proc Natl Acad Sci U S A 103(40):14836-41. [PubMed: 16988010]  [MGI Ref ID J:114699]

Zhu H; Acquaviva J; Ramachandran P; Boskovitz A; Woolfenden S; Pfannl R; Bronson RT; Chen JW; Weissleder R; Housman DE; Charest A. 2009. Oncogenic EGFR signaling cooperates with loss of tumor suppressor gene functions in gliomagenesis. Proc Natl Acad Sci U S A 106(8):2712-6. [PubMed: 19196966]  [MGI Ref ID J:146494]

Zhu HH; Ji K; Alderson N; He Z; Li S; Liu W; Zhang DE; Li L; Feng GS. 2011. Kit-Shp2-Kit signaling acts to maintain a functional hematopoietic stem and progenitor cell pool. Blood 117(20):5350-61. [PubMed: 21450902]  [MGI Ref ID J:177959]

Zou Y; Niu W; Qin S; Downes M; Burns DK; Zhang CL. 2012. The nuclear receptor TLX is required for gliomagenesis within the adult neurogenic niche. Mol Cell Biol 32(23):4811-20. [PubMed: 23028043]  [MGI Ref ID J:192734]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX11

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, these mice are bred as homozygotes.
Mating SystemHomozygote x Homozygote         (Female x Male)   25-JAN-08
Diet Information LabDiet® 5K52/5K67

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $232.00Female or MaleHomozygous for Ptentm1Hwu  
Price per Pair (US dollars $)Pair Genotype
$464.00Homozygous for Ptentm1Hwu x Homozygous for Ptentm1Hwu  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $301.60Female or MaleHomozygous for Ptentm1Hwu  
Price per Pair (US dollars $)Pair Genotype
$603.20Homozygous for Ptentm1Hwu x Homozygous for Ptentm1Hwu  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Control Information

  Control
   000664 C57BL/6J
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.
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Terms of Use

Terms of Use


General Terms and Conditions


For Licensing and Use Restrictions view the link(s) below:
- Use of MICE by companies or for-profit entities requires a license prior to shipping.

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phone:207-288-6470

JAX® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

No Warranty

MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.


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