Strain Name:

B6.129S2-Rb1tm1Tyj/J

Stock Number:

002102

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Availability:

Cryopreserved - Ready for recovery

Use Restrictions Apply, see Terms of Use
Mice homozygous for this targeted mutation die in utero from an apparent failure to produce erythrocytes in the liver. Heterozygous mice develop pituitary tumors by 8 months of age.

Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

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.
Specieslaboratory mouse
Background Strain C57BL/6J
Donor Strain 129S2 via D3 ES cell line
 
Donating Investigator IMR Colony,   The Jackson Laboratory

Appearance
black
Related Genotype: a/a

Description
Mice homozygous for this targeted mutation die in utero, apparently from a failure to produce erythrocytes in the liver, demonstrating that the endogenous gene is essential for normal development. Heterozygous mice, which are analogous to human carrier individuals, do not develop retinal tumors, but do develop pituitary tumors by 8 months of age.

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. This is the case for this strain. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

Development
This mutant strain was developed in the laboratory of Dr. Tyler Jacks at the Center for Cancer Research at the Massachusetts Institute of Technology. The 129-derived D3 ES cell line was used. This strain was made by backcrossing mutant mice at least 5 generations to C57BL/6J.

Control Information

  Control
   Wild-type from the colony
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Rb1tm1Tyj allele
002082   129S-Rb1tm1Tyj/J
002546   C3Ou.129S2-Rb1tm1Tyj/J
002900   FVB.129S2(B6)-Rb1tm1Tyj/J
View Strains carrying   Rb1tm1Tyj     (3 strains)

Strains carrying other alleles of Rb1
008186   B6;129-Rb1tm3Tyj/J
View Strains carrying other alleles of Rb1     (1 strain)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Bladder Cancer   (RB1)
Osteogenic Sarcoma   (RB1)
Retinoblastoma; RB1   (RB1)
Small Cell Cancer of the Lung   (RB1)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

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

Rb1tm1Tyj/Rb1+

        involves: 129S2/SvPas * C57BL/6
  • mortality/aging
  • premature death
    • all heterozygous mutant mice die between 8.5 and 13.9 months of age   (MGI Ref ID J:81082)
  • tumorigenesis
  • *normal* tumorigenesis
    • up to 11 months of age, none of >100 heterozygotes studied show any macroscopic sign of retinoblastoma relative to wild-type mice   (MGI Ref ID J:2511)
    • in addition, no precursor lesions (retinomas) are detected by indirect ophthalmology or histological evaluation   (MGI Ref ID J:2511)
    • increased pituitary gland tumor incidence
      • at autopsy, heterozygotes with severe wasting symptoms show large pituitary adenocarcinomas (~ 6 mm in diameter)   (MGI Ref ID J:2511)
      • consistent with the "two-hit" model proposed by Knudson, such pituitary tumors are shown to arise from cells in which the wild-type allele is absent   (MGI Ref ID J:2511)
      • heterozygotes develop intermediate lobe pituitary tumors   (MGI Ref ID J:81082)
    • increased thyroid tumor incidence
      • 23/27 heterozygotes show c-cell thyroid tumors   (MGI Ref ID J:81082)
  • growth/size/body phenotype
  • cachexia
    • at 8-10 months of age, a number of heterozygotes display severe wasting   (MGI Ref ID J:2511)

Rb1tm1Tyj/Rb1+

        involves: 129S2/SvPas * C57BL/6J
  • mortality/aging
  • premature death
    • median lifespan is 372 days compared to 546 days for Men1tm1.1Ctre heterozygotes   (MGI Ref ID J:133299)
  • tumorigenesis
  • increased lung tumor incidence
    • in 60% of mice   (MGI Ref ID J:133299)
  • increased metastatic potential
    • 60% of mice exhibit lung metastasis   (MGI Ref ID J:133299)
  • increased pheochromocytoma incidence
    • in 40% of mice   (MGI Ref ID J:133299)
  • increased pituitary adenohypophysis tumor incidence
    • mice exhibit tumors of the pituitary anterior lobe (42%)   (MGI Ref ID J:133299)
    • however, no parathyroid adenomas are observed   (MGI Ref ID J:133299)
  • increased pituitary melanotroph tumor incidence
    • all mice exhibit tumors of the pituitary intermediate lobe   (MGI Ref ID J:133299)
  • increased thyroid C-cell carcinoma incidence
    • all mice exhibit metastic thyroid C-cell carcinomas   (MGI Ref ID J:133299)

Rb1tm1Tyj/Rb1+

        involves: 129S2/SvPas * 129S6/SvEvTac * FVB/N
  • mortality/aging
  • premature death
    • median survival is 47 weeks   (MGI Ref ID J:175625)
  • tumorigenesis
  • increased pituitary gland tumor incidence
    • in 9 of 10 mice; 5 of 5 with intermediate lobe origins   (MGI Ref ID J:175625)
  • increased thyroid tumor incidence
    • in 8 of 10 mice   (MGI Ref ID J:175625)

Rb1tm1Tyj/Rb1tm1Tyj

        involves: 129S2/SvPas
  • mortality/aging
  • complete embryonic lethality during organogenesis
    • live homozygotes are rarely recovered at E15.5 and never at E16.5   (MGI Ref ID J:105548)
  • hematopoietic system phenotype
  • abnormal erythropoiesis
    • significant decrease in the percentage of enucleated erythrocytes, indicating defective erythrocyte maturation   (MGI Ref ID J:105548)
    • increased nucleated erythrocyte cell number
      • at E13.5, peripheral blood smears contain predominantly nucleated erythrocytes   (MGI Ref ID J:81643)
  • abnormal macrophage differentiation
    • fetal liver macrophages exhibit defects in differentiation, as indicated by small size, lack of extensive cytoplasmic projections, and weak staining for a mature macrophage marker   (MGI Ref ID J:105548)
  • liver/biliary system phenotype
  • liver hypoplasia
    • at E13.5 liver cellularity is decreased and the level of apoptosis is increased   (MGI Ref ID J:81643)
  • nervous system phenotype
  • abnormal dorsal root ganglion morphology
    • detect ectopic mitosis and apoptosis in the dorsal root ganglia   (MGI Ref ID J:105548)
  • abnormal fourth ventricle morphology
    • detect ectopic mitosis and apoptosis in the intermediate zones of the fourth ventricle   (MGI Ref ID J:105548)
  • abnormal neuron differentiation
    • at E13.5, proliferation is increased in the brain, dorsal root ganglia, and trigeminal ganglia   (MGI Ref ID J:81643)
  • abnormal third ventricle morphology
    • detect ectopic mitosis and apoptosis in the intermediate zones of the third ventricle   (MGI Ref ID J:105548)
  • abnormal trigeminal ganglion morphology
    • detect ectopic mitosis and apoptosis in the trigeminal ganglia   (MGI Ref ID J:105548)
  • increased neuron apoptosis
    • at E13.5, apoptosis is increased in the brain, dorsal root ganglia, and trigeminal ganglia   (MGI Ref ID J:81643)
  • vision/eye phenotype
  • abnormal lens development
    • at E13.5, ectopic proliferating cells are seen in the interior of the lens and increased apoptosis is seen   (MGI Ref ID J:81643)
  • abnormal lens fiber morphology
    • detect ectopic mitoses in the lens fiber compartment that is not seen in wild-type   (MGI Ref ID J:105548)
    • lens fiber cells are disorganized   (MGI Ref ID J:105548)
  • increased lens fiber apoptosis
    • apoptosis is detected in the lens fiber compartment that is not seen in wild-type   (MGI Ref ID J:105548)
  • homeostasis/metabolism phenotype
  • hypoxia
    • expression of hypoxia-inducible genes is increased in the central nervous system at E13.5   (MGI Ref ID J:81643)
  • cellular phenotype
  • abnormal cell cycle
    • MEFs exhibit an increase in the fraction of cells in the S and G2/M phases of the cell cycle   (MGI Ref ID J:105548)
    • abnormal cell cycle checkpoint function
      • MEFs fail to efficiently trigger G1/S cell cycle arrest in response to DNA damage   (MGI Ref ID J:105548)
  • abnormal macrophage differentiation
    • fetal liver macrophages exhibit defects in differentiation, as indicated by small size, lack of extensive cytoplasmic projections, and weak staining for a mature macrophage marker   (MGI Ref ID J:105548)
  • abnormal neuron differentiation
    • at E13.5, proliferation is increased in the brain, dorsal root ganglia, and trigeminal ganglia   (MGI Ref ID J:81643)
  • increased cell proliferation
    • MEFs cultured at confluence exhibit an increase in cell proliferation compared to wild-type MEFs   (MGI Ref ID J:105548)
  • increased lens fiber apoptosis
    • apoptosis is detected in the lens fiber compartment that is not seen in wild-type   (MGI Ref ID J:105548)
  • increased neuron apoptosis
    • at E13.5, apoptosis is increased in the brain, dorsal root ganglia, and trigeminal ganglia   (MGI Ref ID J:81643)
  • embryogenesis phenotype
  • abnormal placenta labyrinth morphology
    • normal labyrinth architecture is disrupted   (MGI Ref ID J:105548)
    • the porous appearance of the labyrinth layer is absent   (MGI Ref ID J:105548)
  • abnormal placental transport
    • exhibit defective placental transport as indicated by a 7.2% reduction of the essential fatty acid linoleic acid, arachidonic acid and docosahexaenoic acid in E14.5 embryos relative to wild-type   (MGI Ref ID J:105548)
  • decreased embryo size   (MGI Ref ID J:105548)
  • growth/size/body phenotype
  • decreased embryo size   (MGI Ref ID J:105548)
  • immune system phenotype
  • abnormal macrophage differentiation
    • fetal liver macrophages exhibit defects in differentiation, as indicated by small size, lack of extensive cytoplasmic projections, and weak staining for a mature macrophage marker   (MGI Ref ID J:105548)
  • integument phenotype
  • pallor   (MGI Ref ID J:105548)

Rb1tm1Tyj/Rb1tm1Tyj

        involves: 129S2/SvPas * C57BL/6
  • mortality/aging
  • complete lethality throughout fetal growth and development   (MGI Ref ID J:81082)
    • homozygous mutant embryos die between E14.5 and E15.5   (MGI Ref ID J:2511)
  • hematopoietic system phenotype
  • abnormal erythropoiesis
    • at E13.5, homozygotes display impaired definitive erythropoiesis and fail to produce sufficient numbers of mature erythrocytes, resulting in hypoxia and eventually death   (MGI Ref ID J:2511)
    • abnormal erythrocyte morphology
      • in vitro, mutant erythroid precursors fail to reach end-stage differentiation: small hemaglobinized colonies from mutant mice are pale and contain increased numbers of small late normoblast-like cells instead of enucleated (mature) erythrocytes   (MGI Ref ID J:2511)
      • similarly, mutant large erythroid colonies are pale, with <5% enucleated erythrocytes relative to wild-type (45%)   (MGI Ref ID J:2511)
      • low mean erythrocyte cell number
        • at E13.5, wild-type embryos contain on average 45% enucleated, definitive erythrocytes; in contrast, mutant embryos only contain 6.8% enucleated cells   (MGI Ref ID J:2511)
  • anemia
    • at E13.5, homozygotes are severely pale relative to wild-type embryos   (MGI Ref ID J:2511)
  • liver/biliary system phenotype
  • abnormal liver morphology
    • at E13.5, mutant livers appear lacy and largely acellular; in contrast, wild-type livers are densely packed with cells (90% of which are of erythroid lineage)   (MGI Ref ID J:2511)
    • small liver
      • at E13.5, homozygotes display a slight reduction in liver size   (MGI Ref ID J:2511)
  • homeostasis/metabolism phenotype
  • pericardial edema
    • at E13.5, homozygotes display significant edema, particularly in the pericardial space   (MGI Ref ID J:2511)
  • skin edema
    • at E13.5, edema results in damage of the dermis and underlying mesenchyme   (MGI Ref ID J:2511)
    • however, most non-hematopoietic tissues remain unaffected until death (~E14.5)   (MGI Ref ID J:2511)
  • cardiovascular system phenotype
  • pericardial edema
    • at E13.5, homozygotes display significant edema, particularly in the pericardial space   (MGI Ref ID J:2511)
  • nervous system phenotype
  • *normal* nervous system phenotype
    • normal numbers of primary neurospheres are produced from cultured E10 telencephalic neuroepithelia   (MGI Ref ID J:92520)
    • increased neuron apoptosis
      • at E12.5, mutant embryos exhibit increased neuronal apoptosis in the spinal cord, dorsal root ganglia and parts of the hindbrain   (MGI Ref ID J:2511)
      • neuronal cell death occurs prior to the manifestation of the erythropoietic defect, and does not appear to be a secondary effect of anemia-induced hypoxia   (MGI Ref ID J:2511)
  • vision/eye phenotype
  • *normal* vision/eye phenotype
    • at 13.5 dpc, homozygotes display normal retinal development at E13.5, homozygotes display normal retinal development   (MGI Ref ID J:2511)
  • cellular phenotype
  • increased apoptosis
    • at E13.5, TUNEL analysis indicates a significant increase in apoptotic nuclei throughout the mutant nervous system (esp. dorsal ganglia), in skeletal muscle precursor cells (e.g. tongue myoblasts), lens, and to a lesser extent in liver   (MGI Ref ID J:37145)
    • in contrast, no significant increase in apoptosis is noted in the mutant lung or cardiac muscles   (MGI Ref ID J:37145)
    • increased neuron apoptosis
      • at E12.5, mutant embryos exhibit increased neuronal apoptosis in the spinal cord, dorsal root ganglia and parts of the hindbrain   (MGI Ref ID J:2511)
      • neuronal cell death occurs prior to the manifestation of the erythropoietic defect, and does not appear to be a secondary effect of anemia-induced hypoxia   (MGI Ref ID J:2511)
  • increased cell proliferation
    • MEFs largely fail to arrest in response to confluent growth and ~40% of the cells enter S phase   (MGI Ref ID J:81082)
  • behavior/neurological phenotype
  • hunched posture
    • at E13.5, 7 of 8 homozygotes display a hunchback posture   (MGI Ref ID J:37145)
  • skeleton phenotype
  • abnormal cartilage morphology
    • at E13.5, 7 of 8 homozygotes display a reduced cartilaginous frame (perichondrium) relative to wild-type mice   (MGI Ref ID J:37145)
  • integument phenotype
  • skin edema
    • at E13.5, edema results in damage of the dermis and underlying mesenchyme   (MGI Ref ID J:2511)
    • however, most non-hematopoietic tissues remain unaffected until death (~E14.5)   (MGI Ref ID J:2511)

Rb1tm1Tyj/Rb1tm1Tyj

        involves: 129S2/SvPas * 129S6/SvEvTac * FVB/N
  • mortality/aging
  • complete embryonic lethality   (MGI Ref ID J:175625)
  • cellular phenotype
  • abnormal cell differentiation
    • mouse embryonic fibroblasts transfected with a vector expressing Myod1 (MyoD) fail to differentiate into myocytes unlike similarly treated wild-type cells   (MGI Ref ID J:175625)
    • transfection with a vector expressing Myhc partially rescues myocyte differentiation   (MGI Ref ID J:175625)
View Research Applications

Research Applications
This mouse can be used to support research in many areas including:

Rb1tm1Tyj related

Apoptosis Research
Endogenous Regulators

Cancer Research
Increased Tumor Incidence
      Other Tissues/Organs
      Other Tissues/Organs: pituitary
Tumor Suppressor Genes
      pituitary tumors

Developmental Biology Research
Internal/Organ Defects
      liver

Hematological Research
Hematopoietic Defects

Immunology, Inflammation and Autoimmunity Research
Intracellular Signaling Molecules

Internal/Organ Research
Liver Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Rb1tm1Tyj
Allele Name targeted mutation 1, Tyler Jacks
Allele Type Targeted (Null/Knockout)
Common Name(s) Rb-; Rb1-; Rbx3t; pRb-;
Mutation Made ByDr. Tyler Jacks,   Massachusetts Institute of Technology
Strain of Origin129S2/SvPas
ES Cell Line NameD3
ES Cell Line Strain129S2/SvPas
Gene Symbol and Name Rb1, retinoblastoma 1
Chromosome 14
Gene Common Name(s) OSRC; PPP1R130; RB; Rb-1; p105-Rb; pRb; pp110;
General Note This is one of several targeted null mutations of Rb1 that have been created. Results appear to be similar for all the mutations (J:2498, J:2511, J:2516). Heterozygotes for the mutations show no predisposition to retinoblastoma. Homozygotes die in utero with neuronal and hematopoietic system abnormalities. Transfer of a human RB1 mini-transgene into the mutant mice corrects the defects (J:2516). On the other hand, transfer of the human gene into mice with a normal Rb1 genotype, causing overexpression of the gene product, produces mice dwarfed in proportion to the number of extra RB1 copies they carry (J:15042).Homozygous Rb1tm1Tyj mutant mice given a transgene producing low levels of Rb1 product survive to birth, but die at that stage due tofailure of myogenesis. Myoblasts undergo massive apoptosis, and surviving cells do not undergo terminal differentiation (J:37145).
Molecular Note A PGK-neomycin resistance cassette replaced part of intron 3 and introduced three nucleotide changes into exon 3, creating two termination codons and a new PstI site. The authors predict translation of a truncated protein by the mutant allele. Immunoblotanalysis of E12.5 brain did not detect full length RB1 protein in homozygous mice. [MGI Ref ID J:2511]

Genotyping

Genotyping Information

Genotyping Protocols

Rb1tm1Tyj,

Separated MCA


NEOTD (Generic Neo), Standard PCR
Rb1tm1Tyj, Separated PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Additional References

Rb1tm1Tyj related

Ajioka I; Martins RA; Bayazitov IT; Donovan S; Johnson DA; Frase S; Cicero SA; Boyd K; Zakharenko SS; Dyer MA. 2007. Differentiated horizontal interneurons clonally expand to form metastatic retinoblastoma in mice. Cell 131(2):378-90. [PubMed: 17956737]  [MGI Ref ID J:130181]

Almeida MQ; Muchow M; Boikos S; Bauer AJ; Griffin KJ; Tsang KM; Cheadle C; Watkins T; Wen F; Starost MF; Bossis I; Nesterova M; Stratakis CA. 2010. Mouse Prkar1a haploinsufficiency leads to an increase in tumors in the Trp53+/- or Rb1+/- backgrounds and chemically induced skin papillomas by dysregulation of the cell cycle and Wnt signaling. Hum Mol Genet 19(8):1387-98. [PubMed: 20080939]  [MGI Ref ID J:158372]

Andreu-Vieyra C; Chen R; Matzuk MM. 2008. Conditional deletion of the retinoblastoma (rb) gene in ovarian granulosa cells leads to premature ovarian failure. Mol Endocrinol 22(9):2141-61. [PubMed: 18599617]  [MGI Ref ID J:138319]

Andreu-Vieyra C; Chen R; Matzuk MM. 2007. Effects of granulosa cell-specific deletion of Rb in Inha-alpha null female mice. Endocrinology 148(8):3837-49. [PubMed: 17510234]  [MGI Ref ID J:123844]

Bajenaru ML; Donahoe J; Corral T; Reilly KM; Brophy S; Pellicer A; Gutmann DH. 2001. Neurofibromatosis 1 (NF1) heterozygosity results in a cell-autonomous growth advantage for astrocytes. Glia 33(4):314-23. [PubMed: 11246230]  [MGI Ref ID J:80411]

Baker DJ; Jin F; Jeganathan KB; van Deursen JM. 2009. Whole chromosome instability caused by Bub1 insufficiency drives tumorigenesis through tumor suppressor gene loss of heterozygosity. Cancer Cell 16(6):475-86. [PubMed: 19962666]  [MGI Ref ID J:155824]

Bakkar N; Wang J; Ladner KJ; Wang H; Dahlman JM; Carathers M; Acharyya S; Rudnicki MA; Hollenbach AD; Guttridge DC. 2008. IKK/NF-kappaB regulates skeletal myogenesis via a signaling switch to inhibit differentiation and promote mitochondrial biogenesis. J Cell Biol 180(4):787-802. [PubMed: 18299349]  [MGI Ref ID J:135692]

Bignon YJ; Chen Y; Chang CY; Riley DJ; Windle JJ; Mellon PL; Lee WH. 1993. Expression of a retinoblastoma transgene results in dwarf mice. Genes Dev 7(9):1654-62. [PubMed: 8370518]  [MGI Ref ID J:15042]

Borges HL; Hunton IC; Wang JY. 2007. Reduction of apoptosis in Rb-deficient embryos via Abl knockout. Oncogene 26(26):3868-77. [PubMed: 17173068]  [MGI Ref ID J:122882]

Bultman SJ; Herschkowitz JI; Godfrey V; Gebuhr TC; Yaniv M; Perou CM; Magnuson T. 2008. Characterization of mammary tumors from Brg1 heterozygous mice. Oncogene 27(4):460-8. [PubMed: 17637742]  [MGI Ref ID J:132091]

Chesnokova V; Kovacs K; Castro AV; Zonis S; Melmed S. 2005. Pituitary hypoplasia in Pttg-/- mice is protective for Rb+/- pituitary tumorigenesis. Mol Endocrinol 19(9):2371-9. [PubMed: 15919720]  [MGI Ref ID J:114916]

Chesnokova V; Zonis S; Kovacs K; Ben-Shlomo A; Wawrowsky K; Bannykh S; Melmed S. 2008. p21(Cip1) restrains pituitary tumor growth. Proc Natl Acad Sci U S A 105(45):17498-503. [PubMed: 18981426]  [MGI Ref ID J:143217]

Chesnokova V; Zonis S; Rubinek T; Yu R; Ben-Shlomo A; Kovacs K; Wawrowsky K; Melmed S. 2007. Senescence mediates pituitary hypoplasia and restrains pituitary tumor growth. Cancer Res 67(21):10564-72. [PubMed: 17975001]  [MGI Ref ID J:127141]

Choi YS; Lee JE; Cheong C; Sung YH; Yang EY; Park CB; Song J; Park SC; Lee HW. 2005. Generation of reversible Rb-knockdown mice. Mech Ageing Dev 126(11):1164-9. [PubMed: 16087217]  [MGI Ref ID J:101661]

Chong JL; Tsai SY; Sharma N; Opavsky R; Price R; Wu L; Fernandez SA; Leone G. 2009. E2f3a and E2f3b contribute to the control of cell proliferation and mouse development. Mol Cell Biol 29(2):414-24. [PubMed: 19015245]  [MGI Ref ID J:144747]

Ciavarra G; Zacksenhaus E. 2010. Rescue of myogenic defects in Rb-deficient cells by inhibition of autophagy or by hypoxia-induced glycolytic shift. J Cell Biol 191(2):291-301. [PubMed: 20937698]  [MGI Ref ID J:165519]

Clark AJ; Doyle KM; Humbert PO. 2004. Cell-intrinsic requirement for pRb in erythropoiesis. Blood 104(5):1324-6. [PubMed: 15155463]  [MGI Ref ID J:92702]

Clarke AR; Maandag ER; van Roon M; van der Lugt NM; van der Valk M; Hooper ML; Berns A; te Riele H. 1992. Requirement for a functional Rb-1 gene in murine development [see comments] Nature 359(6393):328-30. [PubMed: 1406937]  [MGI Ref ID J:2498]

Conkrite K; Sundby M; Mu D; Mukai S; MacPherson D. 2012. Cooperation between Rb and Arf in suppressing mouse retinoblastoma. J Clin Invest 122(5):1726-33. [PubMed: 22484813]  [MGI Ref ID J:184538]

Coschi CH; Martens AL; Ritchie K; Francis SM; Chakrabarti S; Berube NG; Dick FA. 2010. Mitotic chromosome condensation mediated by the retinoblastoma protein is tumor-suppressive. Genes Dev 24(13):1351-63. [PubMed: 20551166]  [MGI Ref ID J:161363]

Coxon AB; Ward JM; Geradts J; Otterson GA; Zajac-Kaye M; Kaye FJ. 1998. RET cooperates with RB/p53 inactivation in a somatic multi-step model for murine thyroid cancer. Oncogene 17(12):1625-8. [PubMed: 9794240]  [MGI Ref ID J:50139]

Dackor J; Strunk KE; Wehmeyer MM; Threadgill DW. 2007. Altered trophoblast proliferation is insufficient to account for placental dysfunction in Egfr null embryos. Placenta 28(11-12):1211-8. [PubMed: 17822758]  [MGI Ref ID J:141339]

Davis JN; McCabe MT; Hayward SW; Park JM; Day ML. 2005. Disruption of Rb/E2F pathway results in increased cyclooxygenase-2 expression and activity in prostate epithelial cells. Cancer Res 65(9):3633-42. [PubMed: 15867358]  [MGI Ref ID J:98347]

De Bruin A; Wu L; Saavedra HI; Wilson P; Yang Y; Rosol TJ; Weinstein M; Robinson ML; Leone G. 2003. Rb function in extraembryonic lineages suppresses apoptosis in the CNS of Rb-deficient mice. Proc Natl Acad Sci U S A 100(11):6546-51. [PubMed: 12732721]  [MGI Ref ID J:83621]

Dirlam A; Spike BT; Macleod KF. 2007. Deregulated E2f-2 underlies cell cycle and maturation defects in retinoblastoma null erythroblasts. Mol Cell Biol 27(24):8713-28. [PubMed: 17923680]  [MGI Ref ID J:129010]

Donangelo I; Gutman S; Horvath E; Kovacs K; Wawrowsky K; Mount M; Melmed S. 2006. Pituitary tumor transforming gene overexpression facilitates pituitary tumor development. Endocrinology 147(10):4781-91. [PubMed: 16809444]  [MGI Ref ID J:113662]

Donangelo I; Melmed S. 2005. Pathophysiology of pituitary adenomas. J Endocrinol Invest 28(11 Suppl):100-5. [PubMed: 16625857]  [MGI Ref ID J:116408]

Donovan SL; Dyer MA. 2004. Developmental defects in Rb-deficient retinae. Vision Res 44(28):3323-33. [PubMed: 15536000]  [MGI Ref ID J:102508]

Donovan SL; Schweers B; Martins R; Johnson D; Dyer MA. 2006. Compensation by tumor suppressor genes during retinal development in mice and humans. BMC Biol 4:14. [PubMed: 16672052]  [MGI Ref ID J:110865]

Eason DD; LeBron C; Coppola D; Moscinski LC; Livingston S; Sutton ET; Blanck G. 2003. Development of CD30+ lymphoproliferative disease in mice lacking interferon regulatory factor-1. Oncogene 22(40):6166-76. [PubMed: 13679855]  [MGI Ref ID J:85972]

Fang M; Simeonova I; Bardot B; Lejour V; Jaber S; Bouarich-Bourimi R; Morin A; Toledo F. 2014. Mdm4 loss in mice expressing a p53 hypomorph alters tumor spectrum without improving survival. Oncogene 33(10):1336-9. [PubMed: 23474762]  [MGI Ref ID J:212378]

Garcia MA; Gallego P; Campagna M; Gonzalez-Santamaria J; Martinez G; Marcos-Villar L; Vidal A; Esteban M; Rivas C. 2009. Activation of NF-kB pathway by virus infection requires Rb expression. PLoS One 4(7):e6422. [PubMed: 19649275]  [MGI Ref ID J:151312]

Guidi CJ; Mudhasani R; Hoover K; Koff A; Leav I; Imbalzano AN; Jones SN. 2006. Functional interaction of the retinoblastoma and ini1/snf5 tumor suppressors in cell growth and pituitary tumorigenesis. Cancer Res 66(16):8076-82. [PubMed: 16912184]  [MGI Ref ID J:112109]

Guo Z; Yikang S; Yoshida H; Mak TW; Zacksenhaus E. 2001. Inactivation of the retinoblastoma tumor suppressor induces apoptosis protease-activating factor-1 dependent and independent apoptotic pathways during embryogenesis. Cancer Res 61(23):8395-400. [PubMed: 11731416]  [MGI Ref ID J:73154]

Harrington EA; Bruce JL; Harlow E; Dyson N. 1998. pRB plays an essential role in cell cycle arrest induced by DNA damage. Proc Natl Acad Sci U S A 95(20):11945-50. [PubMed: 9751770]  [MGI Ref ID J:119775]

Hurford RK Jr; Cobrinik D; Lee MH; Dyson N. 1997. pRB and p107/p130 are required for the regulated expression of different sets of E2F responsive genes. Genes Dev 11(11):1447-63. [PubMed: 9192872]  [MGI Ref ID J:41047]

Iavarone A; King ER; Dai XM; Leone G; Stanley ER; Lasorella A. 2004. Retinoblastoma promotes definitive erythropoiesis by repressing Id2 in fetal liver macrophages. Nature 432(7020):1040-5. [PubMed: 15616565]  [MGI Ref ID J:95106]

Jacks T; Fazeli A; Schmitt EM; Bronson RT; Goodell MA; Weinberg RA. 1992. Effects of an Rb mutation in the mouse [see comments] Nature 359(6393):295-300. [PubMed: 1406933]  [MGI Ref ID J:2511]

Jiang Z; Liang P; Leng R; Guo Z; Liu Y; Liu X; Bubnic S; Keating A; Murray D; Goss P; Zacksenhaus E. 2000. E2F1 and p53 are dispensable, whereas p21(Waf1/Cip1) cooperates with Rb to restrict endoreduplication and apoptosis during skeletal myogenesis Dev Biol 227(1):28-41. [PubMed: 11076674]  [MGI Ref ID J:65679]

Jiang Z; Zacksenhaus E; Gallie BL; Phillips RA. 1997. The retinoblastoma gene family is differentially expressed during embryogenesis. Oncogene 14(15):1789-97. [PubMed: 9150384]  [MGI Ref ID J:39767]

Johnson DA; Zhang J; Frase S; Wilson M; Rodriguez-Galindo C; Dyer MA. 2007. Neuronal differentiation and synaptogenesis in retinoblastoma. Cancer Res 67(6):2701-11. [PubMed: 17363591]  [MGI Ref ID J:120315]

Kalitsis P; Fowler KJ; Griffiths B; Earle E; Chow CW; Jamsen K; Choo KH. 2005. Increased chromosome instability but not cancer predisposition in haploinsufficient Bub3 mice. Genes Chromosomes Cancer 44(1):29-36. [PubMed: 15898111]  [MGI Ref ID J:99580]

Kansara M; Leong HS; Lin DM; Popkiss S; Pang P; Garsed DW; Walkley CR; Cullinane C; Ellul J; Haynes NM; Hicks R; Kuijjer ML; Cleton-Jansen AM; Hinds PW; Smyth MJ; Thomas DM. 2013. Immune response to RB1-regulated senescence limits radiation-induced osteosarcoma formation. J Clin Invest 123(12):5351-60. [PubMed: 24231354]  [MGI Ref ID J:207626]

Keramaris E; Ruzhynsky VA; Callaghan SM; Wong E; Davis RJ; Flavell R; Slack RS; Park DS. 2008. Required roles of Bax and JNKs in central and peripheral nervous system death of retinoblastoma-deficient mice. J Biol Chem 283(1):405-15. [PubMed: 17984095]  [MGI Ref ID J:130256]

Kim YC; Kim SY; Mellado-Gil JM; Yadav H; Neidermyer W; Kamaraju AK; Rane SG. 2011. RB regulates pancreas development by stabilizing Pdx1. EMBO J 30(8):1563-76. [PubMed: 21399612]  [MGI Ref ID J:171241]

Knostman KA; Jhiang SM; Capen CC. 2007. Genetic alterations in thyroid cancer: the role of mouse models. Vet Pathol 44(1):1-14. [PubMed: 17197619]  [MGI Ref ID J:129329]

Lasorella A; Noseda M; Beyna M; Yokota Y; Iavarone A. 2000. Id2 is a retinoblastoma protein target and mediates signalling by Myc oncoproteins. Nature 407(6804):592-8. [PubMed: 11034201]  [MGI Ref ID J:77276]

Lasorella A; Rothschild G; Yokota Y; Russell RG; Iavarone A. 2005. Id2 mediates tumor initiation, proliferation, and angiogenesis in rb mutant mice. Mol Cell Biol 25(9):3563-74. [PubMed: 15831462]  [MGI Ref ID J:97629]

Laurie NA; Donovan SL; Shih CS; Zhang J; Mills N; Fuller C; Teunisse A; Lam S; Ramos Y; Mohan A; Johnson D; Wilson M; Rodriguez-Galindo C; Quarto M; Francoz S; Mendrysa SM; Guy RK; Marine JC; Jochemsen AG; Dyer MA. 2006. Inactivation of the p53 pathway in retinoblastoma. Nature 444(7115):61-6. [PubMed: 17080083]  [MGI Ref ID J:115580]

Lee EY; Cam H; Ziebold U; Rayman JB; Lees JA; Dynlacht BD. 2002. E2F4 loss suppresses tumorigenesis in Rb mutant mice. Cancer Cell 2(6):463-72. [PubMed: 12498715]  [MGI Ref ID J:81082]

Lee EY; Yuan TL; Danielian PS; West JC; Lees JA. 2009. E2F4 cooperates with pRB in the development of extra-embryonic tissues. Dev Biol 332(1):104-15. [PubMed: 19433082]  [MGI Ref ID J:152869]

Lee MH; Williams BO; Mulligan G; Mukai S; Bronson RT; Dyson N; Harlow E; Jacks T. 1996. Targeted disruption of p107: functional overlap between p107 and Rb. Genes Dev 10(13):1621-32. [PubMed: 8682293]  [MGI Ref ID J:34058]

Leung SW; Wloga EH; Castro AF; Nguyen T; Bronson RT; Yamasaki L. 2004. A dynamic switch in Rb+/- mediated neuroendocrine tumorigenesis. Oncogene 23(19):3296-307. [PubMed: 15021915]  [MGI Ref ID J:89741]

Lin W; Cao J; Liu J; Beshiri ML; Fujiwara Y; Francis J; Cherniack AD; Geisen C; Blair LP; Zou MR; Shen X; Kawamori D; Liu Z; Grisanzio C; Watanabe H; Minamishima YA; Zhang Q; Kulkarni RN; Signoretti S; Rodig SJ; Bronson RT; Orkin SH; Tuck DP; Benevolenskaya EV; Meyerson M; Kaelin WG Jr; Yan Q. 2011. Loss of the retinoblastoma binding protein 2 (RBP2) histone demethylase suppresses tumorigenesis in mice lacking Rb1 or Men1. Proc Natl Acad Sci U S A 108(33):13379-86. [PubMed: 21788502]  [MGI Ref ID J:175625]

Liu Y; Clem B; Zuba-Surma EK; El-Naggar S; Telang S; Jenson AB; Wang Y; Shao H; Ratajczak MZ; Chesney J; Dean DC. 2009. Mouse fibroblasts lacking RB1 function form spheres and undergo reprogramming to a cancer stem cell phenotype. Cell Stem Cell 4(4):336-47. [PubMed: 19341623]  [MGI Ref ID J:149842]

Liu Y; Zacksenhaus E. 2000. E2F1 mediates ectopic proliferation and stage-specific p53-dependent apoptosis but not aberrant differentiation in the ocular lens of Rb deficient fetuses. Oncogene 19(52):6065-73. [PubMed: 11146559]  [MGI Ref ID J:66392]

MacPherson D; Sage J; Crowley D; Trumpp A; Bronson RT; Jacks T. 2003. Conditional mutation of Rb causes cell cycle defects without apoptosis in the central nervous system. Mol Cell Biol 23(3):1044-53. [PubMed: 12529408]  [MGI Ref ID J:81643]

Macleod KF; Hu Y; Jacks T. 1996. Loss of Rb activates both p53-dependent and independent cell death pathways in the developing mouse nervous system. EMBO J 15(22):6178-88. [PubMed: 8947040]  [MGI Ref ID J:37025]

Mantela J; Jiang Z; Ylikoski J; Fritzsch B; Zacksenhaus E; Pirvola U. 2005. The retinoblastoma gene pathway regulates the postmitotic state of hair cells of the mouse inner ear. Development 132(10):2377-88. [PubMed: 15843406]  [MGI Ref ID J:98518]

Matoso A; Zhou Z; Hayama R; Flesken-Nikitin A; Nikitin AY. 2008. Cell lineage-specific interactions between Men1 and Rb in neuroendocrine neoplasia. Carcinogenesis 29(3):620-8. [PubMed: 17893233]  [MGI Ref ID J:133299]

Mercader J; Ribot J; Murano I; Feddersen S; Cinti S; Madsen L; Kristiansen K; Bonet ML; Palou A. 2009. Haploinsufficiency of the retinoblastoma protein gene reduces diet-induced obesity, insulin resistance, and hepatosteatosis in mice. Am J Physiol Endocrinol Metab 297(1):E184-93. [PubMed: 19417128]  [MGI Ref ID J:151181]

Morgenbesser SD; Williams BO; Jacks T; DePinho RA. 1994. p53-dependent apoptosis produced by Rb-deficiency in the developing mouse lens [see comments] Nature 371(6492):72-4. [PubMed: 8072529]  [MGI Ref ID J:19995]

Nalam RL; Andreu-Vieyra C; Braun RE; Akiyama H; Matzuk MM. 2009. Retinoblastoma protein plays multiple essential roles in the terminal differentiation of Sertoli cells. Mol Endocrinol 23(11):1900-13. [PubMed: 19819985]  [MGI Ref ID J:154066]

Novitch BG; Spicer DB; Kim PS; Cheung WL; Lassar AB. 1999. pRb is required for MEF2-dependent gene expression as well as cell-cycle arrest during skeletal muscle differentiation. Curr Biol 9(9):449-59. [PubMed: 10322110]  [MGI Ref ID J:54605]

Parisi T; Bronson RT; Lees JA. 2009. Inhibition of pituitary tumors in Rb mutant chimeras through E2f4 loss reveals a key suppressive role for the pRB/E2F pathway in urothelium and ganglionic carcinogenesis. Oncogene 28(4):500-8. [PubMed: 18997819]  [MGI Ref ID J:145896]

Parisi T; Yuan TL; Faust AM; Caron AM; Bronson R; Lees JA. 2007. Selective requirements for E2f3 in the development and tumorigenicity of Rb-deficient chimeric tissues. Mol Cell Biol 27(6):2283-93. [PubMed: 17210634]  [MGI Ref ID J:121512]

Reimann M; Loddenkemper C; Rudolph C; Schildhauer I; Teichmann B; Stein H; Schlegelberger B; Dorken B; Schmitt CA. 2007. The Myc-evoked DNA damage response accounts for treatment resistance in primary lymphomas in vivo. Blood 110(8):2996-3004. [PubMed: 17562874]  [MGI Ref ID J:125810]

Sage J; Miller AL; Perez-Mancera PA; Wysocki JM; Jacks T. 2003. Acute mutation of retinoblastoma gene function is sufficient for cell cycle re-entry. Nature 424(6945):223-8. [PubMed: 12853964]  [MGI Ref ID J:84407]

Schmitt CA; McCurrach ME; de Stanchina E; Wallace-Brodeur RR; Lowe SW. 1999. INK4a/ARF mutations accelerate lymphomagenesis and promote chemoresistance by disabling p53. Genes Dev 13(20):2670-7. [PubMed: 10541553]  [MGI Ref ID J:58293]

Schmitt CA; Wallace-Brodeur RR; Rosenthal CT; McCurrach ME; Lowe SW. 2000. DNA damage responses and chemosensitivity in the E mu-myc mouse lymphoma model. Cold Spring Harb Symp Quant Biol 65:499-510. [PubMed: 12760067]  [MGI Ref ID J:84207]

Serra R; Moses HL. 1995. pRb is necessary for inhibition of N-myc expression by TGF-beta 1 in embryonic lung organ cultures. Development 121(9):3057-66. [PubMed: 7555731]  [MGI Ref ID J:28703]

Shamma A; Suzuki M; Hayashi N; Kobayashi M; Sasaki N; Nishiuchi T; Doki Y; Okamoto T; Kohno S; Muranaka H; Kitajima S; Yamamoto K; Takahashi C. 2013. ATM mediates pRB function to control DNMT1 protein stability and DNA methylation. Mol Cell Biol 33(16):3113-24. [PubMed: 23754744]  [MGI Ref ID J:204567]

Shamma A; Takegami Y; Miki T; Kitajima S; Noda M; Obara T; Okamoto T; Takahashi C. 2009. Rb Regulates DNA damage response and cellular senescence through E2F-dependent suppression of N-ras isoprenylation. Cancer Cell 15(4):255-69. [PubMed: 19345325]  [MGI Ref ID J:147436]

Simpson DS; Mason-Richie NA; Gettler CA; Wikenheiser-Brokamp KA. 2009. Retinoblastoma family proteins have distinct functions in pulmonary epithelial cells in vivo critical for suppressing cell growth and tumorigenesis. Cancer Res 69(22):8733-41. [PubMed: 19887614]  [MGI Ref ID J:154440]

Simpson MT; MacLaurin JG; Xu D; Ferguson KL; Vanderluit JL; Davoli MA; Roy S; Nicholson DW; Robertson GS; Park DS; Slack RS. 2001. Caspase 3 deficiency rescues peripheral nervous system defect in retinoblastoma nullizygous mice. J Neurosci 21(18):7089-98. [PubMed: 11549719]  [MGI Ref ID J:71535]

Spike BT; Dibling BC; Macleod KF. 2007. Hypoxic stress underlies defects in erythroblast islands in the Rb-null mouse. Blood 110(6):2173-81. [PubMed: 17557897]  [MGI Ref ID J:127220]

Spike BT; Dirlam A; Dibling BC; Marvin J; Williams BO; Jacks T; Macleod KF. 2004. The Rb tumor suppressor is required for stress erythropoiesis. EMBO J 23(21):4319-29. [PubMed: 15457215]  [MGI Ref ID J:93304]

Sun H; Chang Y; Schweers B; Dyer MA; Zhang X; Hayward SW; Goodrich DW. 2006. An E2F binding-deficient Rb1 protein partially rescues developmental defects associated with Rb1 nullizygosity. Mol Cell Biol 26(4):1527-37. [PubMed: 16449662]  [MGI Ref ID J:105548]

Sun H; Wang Y; Chinnam M; Zhang X; Hayward SW; Foster BA; Nikitin AY; Wills M; Goodrich DW. 2011. E2f binding-deficient Rb1 protein suppresses prostate tumor progression in vivo. Proc Natl Acad Sci U S A 108(2):704-9. [PubMed: 21187395]  [MGI Ref ID J:169702]

Sung YH; Kim HJ; Devkota S; Roh J; Lee J; Rhee K; Bahk YY; Lee HW. 2010. Pierce1, a novel p53 target gene contributing to the ultraviolet-induced DNA damage response. Cancer Res 70(24):10454-63. [PubMed: 21159655]  [MGI Ref ID J:167598]

Takahashi C; Bronson RT; Socolovsky M; Contreras B; Lee KY; Jacks T; Noda M; Kucherlapati R; Ewen ME. 2003. Rb and N-ras function together to control differentiation in the mouse. Mol Cell Biol 23(15):5256-68. [PubMed: 12861012]  [MGI Ref ID J:84571]

Takahashi C; Contreras B; Bronson RT; Loda M; Ewen ME. 2004. Genetic Interaction between Rb and K-ras in the Control of Differentiation and Tumor Suppression. Mol Cell Biol 24(23):10406-15. [PubMed: 15542848]  [MGI Ref ID J:94087]

Takahashi C; Contreras B; Iwanaga T; Takegami Y; Bakker A; Bronson RT; Noda M; Loda M; Hunt JL; Ewen ME. 2006. Nras loss induces metastatic conversion of Rb1-deficient neuroendocrine thyroid tumor. Nat Genet 38(1):118-23. [PubMed: 16369533]  [MGI Ref ID J:106133]

Tallack MR; Keys JR; Humbert PO; Perkins AC. 2009. EKLF/KLF1 controls cell cycle entry via direct regulation of E2f2. J Biol Chem 284(31):20966-74. [PubMed: 19457859]  [MGI Ref ID J:153105]

Talluri S; Isaac CE; Ahmad M; Henley SA; Francis SM; Martens AL; Bremner R; Dick FA. 2010. A G1 checkpoint mediated by the retinoblastoma protein that is dispensable in terminal differentiation but essential for senescence. Mol Cell Biol 30(4):948-60. [PubMed: 20008551]  [MGI Ref ID J:160500]

TeKippe M; Harrison DE; Chen J. 2003. Expansion of hematopoietic stem cell phenotype and activity in Trp53-null mice. Exp Hematol 31(6):521-7. [PubMed: 12829028]  [MGI Ref ID J:115677]

Tracy K; Dibling BC; Spike BT; Knabb JR; Schumacker P; Macleod KF. 2007. BNIP3 is an RB/E2F target gene required for hypoxia-induced autophagy. Mol Cell Biol 27(17):6229-42. [PubMed: 17576813]  [MGI Ref ID J:125010]

Tsai KY; Hu Y; Macleod KF; Crowley D; Yamasaki L; Jacks T. 1998. Mutation of E2f-1 suppresses apoptosis and inappropriate S phase entry and extends survival of Rb-deficient mouse embryos. Mol Cell 2(3):293-304. [PubMed: 9774968]  [MGI Ref ID J:50085]

Tsai KY; MacPherson D; Rubinson DA; Crowley D; Jacks T. 2002. ARF is not required for apoptosis in Rb mutant mouse embryos. Curr Biol 12(2):159-63. [PubMed: 11818069]  [MGI Ref ID J:73917]

Tsai KY; MacPherson D; Rubinson DA; Nikitin AY; Bronson R; Mercer KL; Crowley D; Jacks T. 2002. ARF mutation accelerates pituitary tumor development in Rb+/- mice. Proc Natl Acad Sci U S A 99(26):16865-70. [PubMed: 12486224]  [MGI Ref ID J:81016]

Vanderluit JL; Ferguson KL; Nikoletopoulou V; Parker M; Ruzhynsky V; Alexson T; McNamara SM; Park DS; Rudnicki M; Slack RS. 2004. p107 regulates neural precursor cells in the mammalian brain. J Cell Biol 166(6):853-63. [PubMed: 15353549]  [MGI Ref ID J:92520]

Vasavada RC; Cozar-Castellano I; Sipula D; Stewart AF. 2007. Tissue-specific deletion of the retinoblastoma protein in the pancreatic beta-cell has limited effects on beta-cell replication, mass, and function. Diabetes 56(1):57-64. [PubMed: 17192465]  [MGI Ref ID J:121935]

Wang H; Bauzon F; Ji P; Xu X; Sun D; Locker J; Sellers RS; Nakayama K; Nakayama KI; Cobrinik D; Zhu L. 2010. Skp2 is required for survival of aberrantly proliferating Rb1-deficient cells and for tumorigenesis in Rb1+/- mice. Nat Genet 42(1):83-8. [PubMed: 19966802]  [MGI Ref ID J:155967]

Wang Y; Hayward SW; Donjacour AA; Young P; Jacks T; Sage J; Dahiya R; Cardiff RD; Day ML; Cunha GR. 2000. Sex hormone-induced carcinogenesis in Rb-deficient prostate tissue Cancer Res 60(21):6008-17. [PubMed: 11085521]  [MGI Ref ID J:66195]

Weiss WA; Aldape K; Mohapatra G; Feuerstein BG; Bishop JM. 1997. Targeted expression of MYCN causes neuroblastoma in transgenic mice. EMBO J 16(11):2985-95. [PubMed: 9214616]  [MGI Ref ID J:41126]

Weiss WA; Burns MJ; Hackett C; Aldape K; Hill JR; Kuriyama H; Kuriyama N; Milshteyn N; Roberts T; Wendland MF; DePinho R; Israel MA. 2003. Genetic determinants of malignancy in a mouse model for oligodendroglioma. Cancer Res 63(7):1589-95. [PubMed: 12670909]  [MGI Ref ID J:82649]

Wenzel PL; Wu L; de Bruin A; Chong JL; Chen WY; Dureska G; Sites E; Pan T; Sharma A; Huang K; Ridgway R; Mosaliganti K; Sharp R; Machiraju R; Saltz J; Yamamoto H; Cross JC; Robinson ML; Leone G. 2007. Rb is critical in a mammalian tissue stem cell population. Genes Dev 21(1):85-97. [PubMed: 17210791]  [MGI Ref ID J:117307]

Wikenheiser-Brokamp KA. 2004. Rb family proteins differentially regulate distinct cell lineages during epithelial development. Development 131(17):4299-310. [PubMed: 15294860]  [MGI Ref ID J:92049]

Wikenheiser-Brokamp KA. 2006. Retinoblastoma family proteins: insights gained through genetic manipulation of mice. Cell Mol Life Sci 63(7-8):767-80. [PubMed: 16465443]  [MGI Ref ID J:108542]

Williams BO; Remington L; Albert DM; Mukai S; Bronson RT; Jacks T. 1994. Cooperative tumorigenic effects of germline mutations in Rb and p53. Nat Genet 7(4):480-4. [PubMed: 7951317]  [MGI Ref ID J:19542]

Williams BO; Schmitt EM; Remington L; Bronson RT; Albert DM; Weinberg RA; Jacks T. 1994. Extensive contribution of Rb-deficient cells to adult chimeric mice with limited histopathological consequences. EMBO J 13(18):4251-9. [PubMed: 7925270]  [MGI Ref ID J:59268]

Wu L; de Bruin A; Saavedra HI; Starovic M; Trimboli A; Yang Y; Opavska J; Wilson P; Thompson JC; Ostrowski MC; Rosol TJ; Woollett LA; Weinstein M; Cross JC; Robinson ML; Leone G. 2003. Extra-embryonic function of Rb is essential for embryonic development and viability. Nature 421(6926):942-7. [PubMed: 12607001]  [MGI Ref ID J:82350]

Xiao H; Goodrich DW. 2005. The retinoblastoma tumor suppressor protein is required for efficient processing and repair of trapped topoisomerase II-DNA-cleavable complexes. Oncogene 24(55):8105-13. [PubMed: 16091739]  [MGI Ref ID J:104415]

Yamasaki L; Bronson R; Williams BO; Dyson NJ; Harlow E; Jacks T. 1998. Loss of E2F-1 reduces tumorigenesis and extends the lifespan of Rb1(+/-)mice. Nat Genet 18(4):360-4. [PubMed: 9537419]  [MGI Ref ID J:47108]

Yang H; Williams BO; Hinds PW; Shih TS; Jacks T; Bronson RT; Livingston DM. 2002. Tumor suppression by a severely truncated species of retinoblastoma protein. Mol Cell Biol 22(9):3103-10. [PubMed: 11940667]  [MGI Ref ID J:75738]

Zacksenhaus E; Jiang Z; Chung D; Marth JD; Phillips RA; Gallie BL. 1996. pRb controls proliferation, differentiation, and death of skeletal muscle cells and other lineages during embryogenesis. Genes Dev 10(23):3051-64. [PubMed: 8957005]  [MGI Ref ID J:37145]

Zhang J; Gray J; Wu L; Leone G; Rowan S; Cepko CL; Zhu X; Craft CM; Dyer MA. 2004. Rb regulates proliferation and rod photoreceptor development in the mouse retina. Nat Genet 36(4):351-60. [PubMed: 14991054]  [MGI Ref ID J:109491]

Zhang J; Schweers B; Dyer MA. 2004. The first knockout mouse model of retinoblastoma. Cell Cycle 3(7):952-9. [PubMed: 15190215]  [MGI Ref ID J:103618]

Zhou C; Wawrowsky K; Bannykh S; Gutman S; Melmed S. 2009. E2F1 induces pituitary tumor transforming gene (PTTG1) expression in human pituitary tumors. Mol Endocrinol 23(12):2000-12. [PubMed: 19837943]  [MGI Ref ID J:154681]

Zhou Z; Flesken-Nikitin A; Levine CG; Shmidt EN; Eng JP; Nikitina EY; Spencer DM; Nikitin AY. 2005. Suppression of melanotroph carcinogenesis leads to accelerated progression of pituitary anterior lobe tumors and medullary thyroid carcinomas in Rb+/- mice. Cancer Res 65(3):787-96. [PubMed: 15705875]  [MGI Ref ID J:96382]

Ziebold U; Lee EY; Bronson RT; Lees JA. 2003. E2F3 loss has opposing effects on different pRB-deficient tumors, resulting in suppression of pituitary tumors but metastasis of medullary thyroid carcinomas. Mol Cell Biol 23(18):6542-52. [PubMed: 12944480]  [MGI Ref ID J:85441]

Ziebold U; Reza T; Caron A; Lees JA. 2001. E2F3 contributes both to the inappropriate proliferation and to the apoptosis arising in Rb mutant embryos. Genes Dev 15(4):386-91. [PubMed: 11230146]  [MGI Ref ID J:67783]

Zoumpoulidou G; Broceno C; Li H; Bird D; Thomas G; Mittnacht S. 2012. Role of the tripartite motif protein 27 in cancer development. J Natl Cancer Inst 104(12):941-52. [PubMed: 22556269]  [MGI Ref ID J:189317]

Health & husbandry

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Health & Colony Maintenance Information

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.

Colony Maintenance

Breeding & HusbandryThe Rb1tm1Tyj strain is maintained by mating heterozygous mice to normal wildtype siblings. Heterozygous mice and normal wildtype siblings may be ordered. Expected coat color from breeding:Black

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


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Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2140.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2782.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Control Information

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   Wild-type from the colony
   000664 C57BL/6J
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.
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Tel: 1-800-422-6423 or 1-207-288-5845
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Terms of Use

Terms of Use


General Terms and Conditions


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

Contact information

General inquiries regarding Terms of Use

Contracts Administration

phone:207-288-6470

JAX® Mice, Products & Services Conditions of Use

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

No Warranty

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

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

No Liability

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

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

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

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


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