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| 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. | |||||||||||||||||||
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Description
Strain Information
Type Congenic; Mutant Strain; Targeted Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Additional information on Congenic nomenclature. Mating System Homozygote x Homozygote (Female x Male) 25-JAN-08 Species laboratory mouse Generation N11F7 (07-MAR-11)
Generation DefinitionsDonating 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.
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
- 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- 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).
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)
Thyroid Carcinoma, Follicular; FTC (PTEN)
Vacterl Association with Hydrocephalus (PTEN)
assigned by genotype
The following phenotype information may relate to a genetic background differing from 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
- prostate gland adenocarcinoma
- prostate adenocarcinoma is seen by 9-10 weeks of age in mutants infected with an adenovirus expressing Cre recombinase (MGI Ref ID J:144810)
- prostate intraepithelial neoplasia
- 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
- 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.
Contact JAX® Services jaxservices@jax.org for customized breeding options.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 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)
- 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 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)
- 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)
- cellular 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 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)
- 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)
Cd19tm1(cre)Cgn/Cd19tm1(cre)Cgn Ptentm1Hwu/Ptentm1Hwu
involves: 129P2/OlaHsd * 129S4/SvJae (conditional)
- immune system phenotype
- *normal* immune system phenotype
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+ Ptentm1Hwu/Ptentm1Hwu
involves: 129 * 129S4/SvJae * BALB/c * C57BL/6 (conditional)
- mortality/aging
- premature death
- 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)
- T cell derived lymphoma
- 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 prostate gland tumor incidence
- 20% of males develop prostate cancer after 4OHT treatment (MGI Ref ID J:130367)
- prostate intraepithelial neoplasia
- prostate intraepithelial neoplasm (PIN) is observed at 4-6 weeks post 4-OHT treatment (MGI Ref ID J:130367)
- malignant tumors
- 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)
- skin squamous cell carcinoma
- 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
- skin squamous cell carcinoma
- 10% of males and 15.4% of females develop squamous cell carcinoma of the epidermis after 4OHT treatment (MGI Ref ID J:130367)
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)
- 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)
- increased liver weight (MGI Ref ID J:160759)
- hepatic steatosis (MGI Ref ID J:160759)
- 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
- 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
- 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)
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)
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
- splenomegaly (MGI Ref ID J:135172)
- 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
- splenomegaly (MGI Ref ID J:135172)
- 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
- hepatomegaly (MGI Ref ID J:135172)
- tumorigenesis
- acute promyelocytic leukemia
- 26% of mutants develop acute myeloid leukemia (MGI Ref ID J:135172)
- increased acute lymphoblastic leukemia incidence
- 74% of mutants develop T-lymphoblastic leukemia (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
- 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)
- craniofacial phenotype
- megacephaly (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)
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)
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
- 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
- abnormal oocyte morphology
- 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
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
- altered response to CNS ischemic injury
- behavior/neurological phenotype
- abnormal response to novel odor
- 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
- 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
- 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
- increased pancreatic beta cell mass
- 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 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
- growth/size 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
- 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)
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
- leukemia
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 (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 * C57BL/6 * BALB/c (conditional)
- homeostasis/metabolism phenotype
- 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)
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
- nervous system phenotype
- increased solitary pulmonary neuroendocrine cell number
- 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
- 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
- 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
- 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 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)
This mouse can be used to support research in many areas including:
Ptentm1Hwu relatedApoptosis Research
Endogenous Regulators
Cancer Research
Genes Regulating Growth and Proliferation
Cell Biology Research
Genes Regulating Growth and Proliferation
Research Tools
Apoptosis Research
Cancer Research
Cre-lox System
loxP-flanked Sequences
Developmental Biology Research
Cre-lox System
Cancer Research
Tumor Suppressor Genes
Cell Biology Research
Cell Cycle Regulation
Genes & Alleles
Gene & Allele Information provided by MGI
| Allele Symbol | Ptentm1Hwu | ||
|---|---|---|---|
| Allele Name | targeted mutation 1, Hong Wu | ||
| Allele Type | Targeted (Floxed/Frt) | ||
| Common Name(s) | PTENF; Ptenex5lox; Ptenfl; Ptenflox; Ptenfx; Ptenlox; Ptenloxp; | ||
| Mutation Made By | Hong Wu, UCLA | ||
| Strain of Origin | 129S4/SvJae | ||
| ES Cell Line Name | LW1 | ||
| ES Cell Line Strain | 129S4/SvJae | ||
| 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; 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 | ||
| 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 relatedAdhikari 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]
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]
Berquin IM; Min Y; Wu R; Wu H; Chen YQ. 2005. Expression signature of the mouse prostate. J Biol Chem 280(43):36442-51. [PubMed: 16055444] [MGI Ref ID J:106938]
Berquin IM; Min Y; Wu R; Wu J; Perry D; Cline JM; Thomas MJ; Thornburg T; Kulik G; Smith A; Edwards IJ; D'Agostino R; Zhang H; Wu H; Kang JX; Chen YQ. 2007. Modulation of prostate cancer genetic risk by omega-3 and omega-6 fatty acids. J Clin Invest 117(7):1866-75. [PubMed: 17607361] [MGI Ref ID J:124208]
Bian Y; Hall B; Sun ZJ; Molinolo A; Chen W; Gutkind JS; Waes CV; Kulkarni AB. 2012. Loss of TGF-beta signaling and PTEN promotes head and neck squamous cell carcinoma through cellular senescence evasion and cancer-related inflammation. Oncogene 31(28):3322-32. [PubMed: 22037217] [MGI Ref ID J:194578]
Bonaguidi MA; Wheeler MA; Shapiro JS; Stadel RP; Sun GJ; Ming GL; Song H. 2011. In vivo clonal analysis reveals self-renewing and multipotent adult neural stem cell characteristics. Cell 145(7):1142-55. [PubMed: 21664664] [MGI Ref ID J:173371]
Boyer A; Paquet M; Lague MN; Hermo L; Boerboom D. 2009. Dysregulation of WNT/CTNNB1 and PI3K/AKT signaling in testicular stromal cells causes granulosa cell tumor of the testis. Carcinogenesis 30(5):869-78. [PubMed: 19237610] [MGI Ref ID J:149060]
Browne CD; Del Nagro CJ; Cato MH; Dengler HS; Rickert RC. 2009. Suppression of phosphatidylinositol 3,4,5-trisphosphate production is a key determinant of B cell anergy. Immunity 31(5):749-60. [PubMed: 19896393] [MGI Ref ID J:155314]
Bun Chan C; Liu X; Pradoldej S; Hao C; An J; Yepes M; Luo HR; Ye K. 2011. Phosphoinositide 3-kinase enhancer regulates neuronal dendritogenesis and survival in neocortex. J Neurosci 31(22):8083-92. [PubMed: 21632930] [MGI Ref ID J:173380]
Burd CE; Sorrentino JA; Clark KS; Darr DB; Krishnamurthy J; Deal AM; Bardeesy N; Castrillon DH; Beach DH; Sharpless NE. 2013. Monitoring tumorigenesis and senescence in vivo with a p16(INK4a)-luciferase model. Cell 152(1-2):340-51. [PubMed: 23332765] [MGI Ref ID J:193498]
Byun DS; Ahmed N; Nasser S; Shin J; Al-Obaidi S; Goel S; Corner GA; Wilson AJ; Flanagan DJ; Williams DS; Augenlicht LH; Vincan E; Mariadason JM. 2011. Intestinal epithelial-specific PTEN inactivation results in tumor formation. Am J Physiol Gastrointest Liver Physiol 301(5):G856-64. [PubMed: 21836055] [MGI Ref ID J:178019]
Cai Z; Simons DL; Fu XY; Feng GS; Wu SM; Zhang X. 2011. Loss of shp2-mediated mitogen-activated protein kinase signaling in muller glial cells results in retinal degeneration. Mol Cell Biol 31(14):2973-83. [PubMed: 21576358] [MGI Ref ID J:174095]
Chen CC; Stairs DB; Boxer RB; Belka GK; Horseman ND; Alvarez JV; Chodosh LA. 2012. Autocrine prolactin induced by the Pten-Akt pathway is required for lactation initiation and provides a direct link between the Akt and Stat5 pathways. Genes Dev 26(19):2154-68. [PubMed: 23028142] [MGI Ref ID J:188260]
Chen J; Li Y; Yu TS; McKay RM; Burns DK; Kernie SG; Parada LF. 2012. A restricted cell population propagates glioblastoma growth after chemotherapy. Nature 488(7412):522-6. [PubMed: 22854781] [MGI Ref ID J:186769]
Chen L; Park SM; Tumanov AV; Hau A; Sawada K; Feig C; Turner JR; Fu YX; Romero IL; Lengyel E; Peter ME. 2010. CD95 promotes tumour growth. Nature 465(7297):492-6. [PubMed: 20505730] [MGI Ref ID J:161953]
Chiao PJ; Ling J. 2011. Kras, Pten, NF-kappaB, and inflammation: dangerous liaisons. Cancer Discov 1(2):103-5. [PubMed: 22586351] [MGI Ref ID J:193072]
Choi N; Zhang B; Zhang L; Ittmann M; Xin L. 2012. Adult Murine Prostate Basal and Luminal Cells Are Self-Sustained Lineages that Can Both Serve as Targets for Prostate Cancer Initiation. Cancer Cell 21(2):253-65. [PubMed: 22340597] [MGI Ref ID J:181459]
Chow DK; Groszer M; Pribadi M; Machniki M; Carmichael ST; Liu X; Trachtenberg JT. 2009. Laminar and compartmental regulation of dendritic growth in mature cortex. Nat Neurosci 12(2):116-8. [PubMed: 19151711] [MGI Ref ID J:145970]
Colombo S; Champeval D; Rambow F; Larue L. 2012. Transcriptomic analysis of mouse embryonic skin cells reveals previously unreported genes expressed in melanoblasts. J Invest Dermatol 132(1):170-8. [PubMed: 21850021] [MGI Ref ID J:180641]
Conley-LaComb MK; Huang W; Wang S; Shi D; Jung YS; Najy A; Fridman R; Bonfil RD; Cher ML; Chen YQ; Kim HR. 2012. PTEN regulates PDGF ligand switch for beta-PDGFR signaling in prostate cancer. Am J Pathol 180(3):1017-27. [PubMed: 22209699] [MGI Ref ID J:181962]
Costa PM; Cardoso AL; Pereira de Almeida LF; Bruce JN; Canoll P; Pedroso de Lima MC. 2012. PDGF-B-mediated downregulation of miR-21: new insights into PDGF signaling in glioblastoma. Hum Mol Genet 21(23):5118-30. [PubMed: 22922228] [MGI Ref ID J:188925]
Couto SS; Cao M; Duarte PC; Banach-Petrosky W; Wang S; Romanienko P; Wu H; Cardiff RD; Abate-Shen C; Cunha GR. 2009. Simultaneous haploinsufficiency of Pten and Trp53 tumor suppressor genes accelerates tumorigenesis in a mouse model of prostate cancer. Differentiation 77(1):103-11. [PubMed: 19281769] [MGI Ref ID J:147066]
Daikoku T; Hirota Y; Tranguch S; Joshi AR; DeMayo FJ; Lydon JP; Ellenson LH; Dey SK. 2008. Conditional loss of uterine Pten unfailingly and rapidly induces endometrial cancer in mice. Cancer Res 68(14):5619-27. [PubMed: 18632614] [MGI Ref ID J:139053]
Daikoku T; Tranguch S; Trofimova IN; Dinulescu DM; Jacks T; Nikitin AY; Connolly DC; Dey SK. 2006. Cyclooxygenase-1 is overexpressed in multiple genetically engineered mouse models of epithelial ovarian cancer. Cancer Res 66(5):2527-31. [PubMed: 16510568] [MGI Ref ID J:106703]
Dave V; Wert SE; Tanner T; Thitoff AR; Loudy DE; Whitsett JA. 2008. Conditional deletion of Pten causes bronchiolar hyperplasia. Am J Respir Cell Mol Biol 38(3):337-45. [PubMed: 17921358] [MGI Ref ID J:146355]
Diallo-Krou E; Yu J; Colby LA; Inoki K; Wilkinson JE; Thomas DG; Giordano TJ; Koenig RJ. 2009. Paired box gene 8-peroxisome proliferator-activated receptor-gamma fusion protein and loss of phosphatase and tensin homolog synergistically cause thyroid hyperplasia in transgenic mice. Endocrinology 150(11):5181-90. [PubMed: 19797117] [MGI Ref ID J:158236]
Diaz-Ruiz O; Zapata A; Shan L; Zhang Y; Tomac AC; Malik N; de la Cruz F; Backman CM. 2009. Selective deletion of PTEN in dopamine neurons leads to trophic effects and adaptation of striatal medium spiny projecting neurons. PLoS One 4(9):e7027. [PubMed: 19750226] [MGI Ref ID J:153622]
Dinulescu DM; Ince TA; Quade BJ; Shafer SA; Crowley D; Jacks T. 2005. Role of K-ras and Pten in the development of mouse models of endometriosis and endometrioid ovarian cancer. Nat Med 11(1):63-70. [PubMed: 15619626] [MGI Ref ID J:96296]
Dobson ME; Diallo-Krou E; Grachtchouk V; Yu J; Colby LA; Wilkinson JE; Giordano TJ; Koenig RJ. 2011. Pioglitazone Induces a Proadipogenic Antitumor Response in Mice with PAX8-PPAR{gamma} Fusion Protein Thyroid Carcinoma. Endocrinology 152(11):4455-65. [PubMed: 21952241] [MGI Ref ID J:177181]
Dourdin N; Schade B; Lesurf R; Hallett M; Munn RJ; Cardiff RD; Muller WJ. 2008. Phosphatase and tensin homologue deleted on chromosome 10 deficiency accelerates tumor induction in a mouse model of ErbB-2 mammary tumorigenesis. Cancer Res 68(7):2122-31. [PubMed: 18381417] [MGI Ref ID J:133305]
Duy C; Hurtz C; Shojaee S; Cerchietti L; Geng H; Swaminathan S; Klemm L; Kweon SM; Nahar R; Braig M; Park E; Kim YM; Hofmann WK; Herzog S; Jumaa H; Koeffler HP; Yu JJ; Heisterkamp N; Graeber TG; Wu H; Ye BH; Melnick A; Muschen M. 2011. BCL6 enables Ph+ acute lymphoblastic leukaemia cells to survive BCR-ABL1 kinase inhibition. Nature 473(7347):384-8. [PubMed: 21593872] [MGI Ref ID J:172636]
Ellwood-Yen K; Keilhack H; Kunii K; Dolinski B; Connor Y; Hu K; Nagashima K; O'Hare E; Erkul Y; Di Bacco A; Gargano D; Shomer NH; Angagaw M; Leccese E; Andrade P; Hurd M; Shin MK; Vogt TF; Northrup A; Bobkova EV; Kasibhatla S; Bronson RT; Scott ML; Draetta G; Richon V; Kohl N; Blume-Jensen P; Andersen JN; Kraus M. 2011. PDK1 Attenuation Fails to Prevent Tumor Formation in PTEN-Deficient Transgenic Mouse Models. Cancer Res 71(8):3052-65. [PubMed: 21493594] [MGI Ref ID J:170965]
Fan HY; Liu Z; Cahill N; Richards JS. 2008. Targeted disruption of pten in ovarian granulosa cells enhances ovulation and extends the life span of luteal cells. Mol Endocrinol 22(9):2128-40. [PubMed: 18606860] [MGI Ref ID J:138315]
Fenton TR; Nathanson D; Ponte de Albuquerque C; Kuga D; Iwanami A; Dang J; Yang H; Tanaka K; Oba-Shinjo SM; Uno M; del Mar Inda M; Wykosky J; Bachoo RM; James CD; DePinho RA; Vandenberg SR; Zhou H; Marie SK; Mischel PS; Cavenee WK; Furnari FB. 2012. Resistance to EGF receptor inhibitors in glioblastoma mediated by phosphorylation of the PTEN tumor suppressor at tyrosine 240. Proc Natl Acad Sci U S A 109(35):14164-9. [PubMed: 22891331] [MGI Ref ID J:188576]
Floc'h N; Kinkade CW; Kobayashi T; Aytes A; Lefebvre C; Mitrofanova A; Cardiff RD; Califano A; Shen MM; Abate-Shen C. 2012. Dual targeting of the Akt/mTOR signaling pathway inhibits castration-resistant prostate cancer in a genetically engineered mouse model. Cancer Res 72(17):4483-93. [PubMed: 22815528] [MGI Ref ID J:191334]
Freeman D; Lesche R; Kertesz N; Wang S; Li G; Gao J; Groszer M; Martinez-Diaz H; Rozengurt N; Thomas G; Liu X; Wu H. 2006. Genetic background controls tumor development in PTEN-deficient mice. Cancer Res 66(13):6492-6. [PubMed: 16818619] [MGI Ref ID J:110567]
Frew IJ; Minola A; Georgiev S; Hitz M; Moch H; Richard S; Vortmeyer AO; Krek W. 2008. Combined VHLH and PTEN mutation causes genital tract cystadenoma and squamous metaplasia. Mol Cell Biol 28(14):4536-48. [PubMed: 18474617] [MGI Ref ID J:137442]
Frew IJ; Thoma CR; Georgiev S; Minola A; Hitz M; Montani M; Moch H; Krek W. 2008. pVHL and PTEN tumour suppressor proteins cooperatively suppress kidney cyst formation. EMBO J 27(12):1747-57. [PubMed: 18497742] [MGI Ref ID J:137073]
Fu Y; Wey S; Wang M; Ye R; Liao CP; Roy-Burman P; Lee AS. 2008. Pten null prostate tumorigenesis and AKT activation are blocked by targeted knockout of ER chaperone GRP78/BiP in prostate epithelium. Proc Natl Acad Sci U S A 105(49):19444-9. [PubMed: 19033462] [MGI Ref ID J:142106]
Furumoto Y; Charles N; Olivera A; Leung WH; Dillahunt S; Sargent JL; Tinsley K; Odom S; Scott E; Wilson TM; Ghoreschi K; Kneilling M; Chen M; Lee DM; Bolland S; Rivera J. 2011. PTEN deficiency in mast cells causes a mastocytosis-like proliferative disease that heightens allergic responses and vascular permeability. Blood 118(20):5466-75. [PubMed: 21926349] [MGI Ref ID J:178784]
Ghosh S; Lau H; Simons BW; Powell JD; Meyers DJ; De Marzo AM; Berman DM; Lotan TL. 2011. PI3K/mTOR signaling regulates prostatic branching morphogenesis. Dev Biol 360(2):329-42. [PubMed: 22015718] [MGI Ref ID J:178714]
Goebbels S; Oltrogge JH; Kemper R; Heilmann I; Bormuth I; Wolfer S; Wichert SP; Mobius W; Liu X; Lappe-Siefke C; Rossner MJ; Groszer M; Suter U; Frahm J; Boretius S; Nave KA. 2010. Elevated phosphatidylinositol 3,4,5-trisphosphate in glia triggers cell-autonomous membrane wrapping and myelination. J Neurosci 30(26):8953-64. [PubMed: 20592216] [MGI Ref ID J:161841]
Goel HL; Chang C; Pursell B; Leav I; Lyle S; Xi HS; Hsieh CC; Adisetiyo H; Roy-Burman P; Coleman IM; Nelson PS; Vessella RL; Davis RJ; Plymate SR; Mercurio AM. 2012. VEGF/neuropilin-2 regulation of Bmi-1 and consequent repression of IGF-IR define a novel mechanism of aggressive prostate cancer. Cancer Discov 2(10):906-21. [PubMed: 22777769] [MGI Ref ID J:193157]
Goertz MJ; Wu Z; Gallardo TD; Hamra FK; Castrillon DH. 2011. Foxo1 is required in mouse spermatogonial stem cells for their maintenance and the initiation of spermatogenesis. J Clin Invest 121(9):3456-66. [PubMed: 21865646] [MGI Ref ID J:178240]
Gregorian C ; Nakashima J ; Le Belle J ; Ohab J ; Kim R ; Liu A ; Smith KB ; Groszer M ; Garcia AD ; Sofroniew MV ; Carmichael ST ; Kornblum HI ; Liu X ; Wu H. 2009. Pten deletion in adult neural stem/progenitor cells enhances constitutive neurogenesis. J Neurosci 29(6):1874-86. [PubMed: 19211894] [MGI Ref ID J:146630]
Gregorian C; Nakashima J; Dry SM; Nghiemphu PL; Smith KB; Ao Y; Dang J; Lawson G; Mellinghoff IK; Mischel PS; Phelps M; Parada LF; Liu X; Sofroniew MV; Eilber FC; Wu H. 2009. PTEN dosage is essential for neurofibroma development and malignant transformation. Proc Natl Acad Sci U S A 106(46):19479-84. [PubMed: 19846776] [MGI Ref ID J:154673]
Groszer M; Erickson R; Scripture-Adams DD; Dougherty JD; Le Belle J; Zack JA; Geschwind DH; Liu X; Kornblum HI; Wu H. 2006. PTEN negatively regulates neural stem cell self-renewal by modulating G0-G1 cell cycle entry. Proc Natl Acad Sci U S A 103(1):111-116. [PubMed: 16373498] [MGI Ref ID J:104566]
Groszer M; Erickson R; Scripture-Adams DD; Lesche R; Trumpp A; Zack JA; Kornblum HI; Liu X; Wu H. 2001. Negative regulation of neural stem/progenitor cell proliferation by the Pten tumor suppressor gene in vivo. Science 294(5549):2186-9. [PubMed: 11691952] [MGI Ref ID J:73255]
Gu Y; Lindner J; Kumar A; Yuan W; Magnuson MA. 2011. Rictor/mTORC2 is essential for maintaining a balance between beta-cell proliferation and cell size. Diabetes 60(3):827-37. [PubMed: 21266327] [MGI Ref ID J:170129]
Guertin DA; Stevens DM; Saitoh M; Kinkel S; Crosby K; Sheen JH; Mullholland DJ; Magnuson MA; Wu H; Sabatini DM. 2009. mTOR complex 2 is required for the development of prostate cancer induced by Pten loss in mice. Cancer Cell 15(2):148-59. [PubMed: 19185849] [MGI Ref ID J:144810]
Guha M; Plescia J; Leav I; Li J; Languino LR; Altieri DC. 2009. Endogenous tumor suppression mediated by PTEN involves survivin gene silencing. Cancer Res 69(12):4954-8. [PubMed: 19470765] [MGI Ref ID J:149666]
Guo W; Lasky JL; Chang CJ; Mosessian S; Lewis X; Xiao Y; Yeh JE; Chen JY; Iruela-Arispe ML; Varella-Garcia M; Wu H. 2008. Multi-genetic events collaboratively contribute to Pten-null leukaemia stem-cell formation. Nature 453(7194):529-33. [PubMed: 18463637] [MGI Ref ID J:135172]
Guo W; Schubbert S; Chen JY; Valamehr B; Mosessian S; Shi H; Dang NH; Garcia C; Theodoro MF; Varella-Garcia M; Wu H. 2011. Suppression of leukemia development caused by PTEN loss. Proc Natl Acad Sci U S A 108(4):1409-14. [PubMed: 21212363] [MGI Ref ID J:168259]
Hand TW; Cui W; Jung YW; Sefik E; Joshi NS; Chandele A; Liu Y; Kaech SM. 2010. Differential effects of STAT5 and PI3K/AKT signaling on effector and memory CD8 T-cell survival. Proc Natl Acad Sci U S A 107(38):16601-6. [PubMed: 20823247] [MGI Ref ID J:164425]
He L; Hou X; Kanel G; Zeng N; Galicia V; Wang Y; Yang J; Wu H; Birnbaum MJ; Stiles BL. 2010. The critical role of AKT2 in hepatic steatosis induced by PTEN loss. Am J Pathol 176(5):2302-8. [PubMed: 20348245] [MGI Ref ID J:160759]
He XC; Yin T; Grindley JC; Tian Q; Sato T; Tao WA; Dirisina R; Porter-Westpfahl KS; Hembree M; Johnson T; Wiedemann LM; Barrett TA; Hood L; Wu H; Li L. 2007. PTEN-deficient intestinal stem cells initiate intestinal polyposis. Nat Genet 39(2):189-98. [PubMed: 17237784] [MGI Ref ID J:118329]
Hill R; Calvopina JH; Kim C; Wang Y; Dawson DW; Donahue TR; Dry S; Wu H. 2010. PTEN loss accelerates KrasG12D-induced pancreatic cancer development. Cancer Res 70(18):7114-24. [PubMed: 20807812] [MGI Ref ID J:164210]
Hill R; Song Y; Cardiff RD; Van Dyke T. 2005. Heterogeneous tumor evolution initiated by loss of pRb function in a preclinical prostate cancer model. Cancer Res 65(22):10243-54. [PubMed: 16288012] [MGI Ref ID J:103408]
Hsieh AC; Liu Y; Edlind MP; Ingolia NT; Janes MR; Sher A; Shi EY; Stumpf CR; Christensen C; Bonham MJ; Wang S; Ren P; Martin M; Jessen K; Feldman ME; Weissman JS; Shokat KM; Rommel C; Ruggero D. 2012. The translational landscape of mTOR signalling steers cancer initiation and metastasis. Nature 485(7396):55-61. [PubMed: 22367541] [MGI Ref ID J:183775]
Hu Z; Wang H; Lee IH; Modi S; Wang X; Du J; Mitch WE. 2010. PTEN inhibition improves muscle regeneration in mice fed a high-fat diet. Diabetes 59(6):1312-20. [PubMed: 20200318] [MGI Ref ID J:169364]
Hubner A; Mulholland DJ; Standen CL; Karasarides M; Cavanagh-Kyros J; Barrett T; Chi H; Greiner DL; Tournier C; Sawyers CL; Flavell RA; Wu H; Davis RJ. 2012. JNK and PTEN cooperatively control the development of invasive adenocarcinoma of the prostate. Proc Natl Acad Sci U S A 109(30):12046-51. [PubMed: 22753496] [MGI Ref ID J:186492]
Hurtz C; Hatzi K; Cerchietti L; Braig M; Park E; Kim YM; Herzog S; Ramezani-Rad P; Jumaa H; Muller MC; Hofmann WK; Hochhaus A; Ye BH; Agarwal A; Druker BJ; Shah NP; Melnick AM; Muschen M. 2011. BCL6-mediated repression of p53 is critical for leukemia stem cell survival in chronic myeloid leukemia. J Exp Med 208(11):2163-74. [PubMed: 21911423] [MGI Ref ID J:178790]
Huse JT; Holland EC. 2009. Genetically engineered mouse models of brain cancer and the promise of preclinical testing. Brain Pathol 19(1):132-43. [PubMed: 19076778] [MGI Ref ID J:173443]
Iwanaga K; Yang Y; Raso MG; Ma L; Hanna AE; Thilaganathan N; Moghaddam S; Evans CM; Li H; Cai WW; Sato M; Minna JD; Wu H; Creighton CJ; Demayo FJ; Wistuba II; Kurie JM. 2008. Pten inactivation accelerates oncogenic K-ras-initiated tumorigenesis in a mouse model of lung cancer. Cancer Res 68(4):1119-27. [PubMed: 18281487] [MGI Ref ID J:131721]
Jagarlamudi K; Liu L; Adhikari D; Reddy P; Idahl A; Ottander U; Lundin E; Liu K. 2009. Oocyte-specific deletion of Pten in mice reveals a stage-specific function of PTEN/PI3K signaling in oocytes in controlling follicular activation. PLoS One 4(7):e6186. [PubMed: 19587782] [MGI Ref ID J:151696]
Jia S; Gao X; Lee SH; Maira SM; Wu X; Stack EC; Signoretti S; Loda M; Zhao JJ; Roberts TM. 2013. Opposing effects of androgen deprivation and targeted therapy on prostate cancer prevention. Cancer Discov 3(1):44-51. [PubMed: 23258246] [MGI Ref ID J:194362]
Jia S; Liu Z; Zhang S; Liu P; Zhang L; Lee SH; Zhang J; Signoretti S; Loda M; Roberts TM; Zhao JJ. 2008. Essential roles of PI(3)K-p110beta in cell growth, metabolism and tumorigenesis. Nature 454(7205):776-9. [PubMed: 18594509] [MGI Ref ID J:138565]
John GB; Gallardo TD; Shirley LJ; Castrillon DH. 2008. Foxo3 is a PI3K-dependent molecular switch controlling the initiation of oocyte growth. Dev Biol 321(1):197-204. [PubMed: 18601916] [MGI Ref ID J:138697]
Joshi A; Ellenson LH. 2011. Adenovirus mediated homozygous endometrial epithelial Pten deletion results in aggressive endometrial carcinoma. Exp Cell Res 317(11):1580-9. [PubMed: 21397598] [MGI Ref ID J:174151]
Jun HJ; Acquaviva J; Chi D; Lessard J; Zhu H; Woolfenden S; Bronson RT; Pfannl R; White F; Housman DE; Iyer L; Whittaker CA; Boskovitz A; Raval A; Charest A. 2012. Acquired MET expression confers resistance to EGFR inhibition in a mouse model of glioblastoma multiforme. Oncogene 31(25):3039-50. [PubMed: 22020333] [MGI Ref ID J:186125]
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Health & husbandry
Health & Colony Maintenance Information
Animal Health Reports
Room Number AX12
Colony Maintenance
Breeding & Husbandry When maintaining a live colony, these mice are bred as homozygotes. Mating System Homozygote 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 |
|
Live Mice
Price per mouse (US dollars $) Gender Genotypes Provided Individual Mouse $177.00 Female or Male Homozygous for Ptentm1Hwu
Price per Pair (US dollars $) Pair Genotype $354.00 Homozygous for Ptentm1Hwu x Homozygous for Ptentm1Hwu Standard Supply
Repository-Live. Repository-Live represents an exclusive set of over 1500 unique mouse models maintained at The Jackson Laboratory to support a vast array of research areas. The breeding colonies for Repository Strains provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. Repository-live orders are treated as custom orders. Within 2 business days, we respond to each availability inquiry or order with various delivery options. Repository Strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping.
| Pricing for International shipping destinations |
|
Live Mice
Price per mouse (US dollars $) Gender Genotypes Provided Individual Mouse $230.10 Female or Male Homozygous for Ptentm1Hwu
Price per Pair (US dollars $) Pair Genotype $460.20 Homozygous for Ptentm1Hwu x Homozygous for Ptentm1Hwu Standard Supply
Repository-Live. Repository-Live represents an exclusive set of over 1500 unique mouse models maintained at The Jackson Laboratory to support a vast array of research areas. The breeding colonies for Repository Strains provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. Repository-live orders are treated as custom orders. Within 2 business days, we respond to each availability inquiry or order with various delivery options. Repository Strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping.
|
|
|
Standard Supply
Repository-Live. Repository-Live represents an exclusive set of over 1500 unique mouse models maintained at The Jackson Laboratory to support a vast array of research areas. The breeding colonies for Repository Strains provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. Repository-live orders are treated as custom orders. Within 2 business days, we respond to each availability inquiry or order with various delivery options. Repository Strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping.
General Supply Notes
- Genomic DNA is available for this strain from the Mouse DNA Resource.
Control Information
| Control | ||
|---|---|---|
| 000664 C57BL/6J | ||
| Considerations for Choosing Controls | ||
| Control Pricing Information for Genetically Engineered Mutant Strains. | ||
Payment Terms and Conditions
Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.
See Terms of Use tab for General Terms and Conditions
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.Ordering Information
JAX® Mice
Surgical and Preconditioning Services
JAX® Services
Customer Services and Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
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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.
Contact information
General inquiries regarding Terms of UseContracts Administration
| phone: | 207-288-6470 |
| fax: | 207-288-6655 |
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.