JAX
Mouse Strain Datasheet - 002900
FVB.129S2(B6)-Rb1tm1Tyj/J
Also Known As: Rbx3t
These Rb1 knock-out mice exhibit neuronal cell death and defective erythropoiesis. They are suitable for use in applications related to the study of retinoblastoma.
Donating Investigator
IMR Colony, The Jackson Laboratory
Genetic overview
| Genetic Background | Generation |
|---|---|
|
FVB/J |
|
Rb1tm1Tyj
| Allele Type | Gene Symbol | Gene Name |
|---|---|---|
| Targeted (Null/Knockout) | Rb1 | RB transcriptional corepressor 1 |
Research Applications
- Apoptosis Research
- Cancer Research
- Developmental Biology Research
- Hematological Research
- Immunology, Inflammation and Autoimmunity Research
- Internal/Organ Research
Detailed Description
Mice homozygous for this targeted mutation die in utero. Homozygous embryos are morphologically indistinguishable from normal embryos at 12.5 days post coitum, but then die between 13.5 d.p.c and 14.5 d.p.c. Defects are seen in fetal liver hematopoiesis as well as in lens and nervous system 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.
Control Suggestions
Selected References
- 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: 1406933MGI: J:2511
Rb1tm1Tyj
Allele Symbol: Rb1tm1Tyj
| Allele Name | targeted mutation 1, Tyler Jacks |
|---|---|
| Allele Type | Targeted (Null/Knockout) |
| Allele Synonym(s) | Rb-; Rb1-; Rbx3t; pRb- |
| Gene Symbol and Name | Rb1, RB transcriptional corepressor 1 |
| Gene Synonym(s) | OSRC; PPP1R130; RB; Rb; Rb-1; Rb-1; p105-Rb; pRb; pp110; retinoblastoma 1 |
| Strain of Origin | 129S2/SvPas |
| Chromosome | 14 |
| 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 to failure 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. Immunoblot analysis of E12.5 brain did not detect full length RB1 protein in homozygous mice. |
| Mutations Made By | Dr. Tyler Jacks, Massachusetts Institute of Technology |
Disease Terms
Research Areas By Genotype
This mouse can be used to support research in many areas including:
Genotype: Rb1tm1Tyj related
- Apoptosis Research
- Endogenous Regulators
- Cancer Research
- Increased Tumor Incidence
- Other Tissues/Organs
- Other Tissues/Organs: pituitary
- Tumor Suppressor Genes
- pituitary tumors
- Increased Tumor Incidence
- Developmental Biology Research
- Internal/Organ Defects
- liver
- Internal/Organ Defects
- Hematological Research
- Hematopoietic Defects
- Immunology, Inflammation and Autoimmunity Research
- Intracellular Signaling Molecules
- Internal/Organ Research
- Liver Defects
Mammalian Phenotype Terms by Genotype
The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain
Genotype: Rb1tm1Tyj/Rb1+
involves: 129S2/SvPas
endocrine/exocrine gland phenotype
- increased pituitary gland tumor incidence
- mice develop pituitary gland tumors with a mean survival of 400 days (MGI Ref ID J:215358)
nervous system phenotype
- increased pituitary gland tumor incidence
- mice develop pituitary gland tumors with a mean survival of 400 days (MGI Ref ID J:215358)
mortality/aging
- postnatal lethality, incomplete penetrance
- mice develop pituitary gland tumors with a mean survival of 400 days (MGI Ref ID J:215358)
neoplasm
- increased pituitary gland tumor incidence
- mice develop pituitary gland tumors with a mean survival of 400 days (MGI Ref ID J:215358)
Genotype: Rb1tm1Tyj/Rb1+
involves: 129S2/SvPas * C57BL/6
endocrine/exocrine gland phenotype
- 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)
nervous system phenotype
- 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)
mortality/aging
- premature death
- all heterozygous mutant mice die between 8.5 and 13.9 months of age (MGI Ref ID J:81082)
neoplasm
- 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)
- neoplasm
growth/size/body region phenotype
- cachexia
- at 8-10 months of age, a number of heterozygotes display severe wasting (MGI Ref ID J:2511)
Genotype: Rb1tm1Tyj/Rb1+
involves: 129S2/SvPas * C57BL/6J
respiratory system phenotype
- increased lung tumor incidence
- in 60% of mice (MGI Ref ID J:133299)
endocrine/exocrine gland phenotype
- increased pheochromocytoma incidence
- in 40% of mice (MGI Ref ID J:133299)
- increased pituitary adenohypophysis tumor incidence
- 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)
nervous system phenotype
- increased pituitary adenohypophysis tumor incidence
- increased pituitary melanotroph tumor incidence
- all mice exhibit tumors of the pituitary intermediate lobe (MGI Ref ID J:133299)
mortality/aging
- premature death
- median lifespan is 372 days compared to 546 days for Men1tm1.1Ctre heterozygotes (MGI Ref ID J:133299)
neoplasm
- 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
- 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)
Genotype: Rb1tm1Tyj/Rb1+
involves: 129S2/SvPas * 129S6/SvEvTac * FVB/N
endocrine/exocrine gland phenotype
- 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)
nervous system phenotype
- increased pituitary gland tumor incidence
- in 9 of 10 mice; 5 of 5 with intermediate lobe origins (MGI Ref ID J:175625)
mortality/aging
- premature death
- median survival is 47 weeks (MGI Ref ID J:175625)
neoplasm
- 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)
Genotype: Rb1tm1Tyj/Rb1tm1Tyj
involves: 129S2/SvPas
mortality/aging
- embryonic lethality during organogenesis, complete penetrance
- live homozygotes are rarely recovered at E15.5 and never at E16.5 (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)
hematopoietic system phenotype
- abnormal erythropoiesis
- significant decrease in the percentage of enucleated erythrocytes, indicating defective erythrocyte maturation (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)
- increased nucleated erythrocyte cell number
- at E13.5, peripheral blood smears contain predominantly nucleated erythrocytes (MGI Ref ID J:81643)
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
- 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 fibroblast 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)
embryo phenotype
- abnormal placenta labyrinth morphology
- 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 region phenotype
- decreased embryo size
- (MGI Ref ID J:105548)
Genotype: Rb1tm1Tyj/Rb1tm1Tyj
involves: 129S2/SvPas * 129S6/SvEvTac * FVB/N
mortality/aging
- embryonic lethality, complete penetrance
- (MGI Ref ID J:175625)
cellular phenotype
- abnormal cell differentiation
Genotype: Rb1tm1Tyj/Rb1tm1Tyj
involves: 129S2/SvPas * C57BL/6
mortality/aging
- lethality throughout fetal growth and development, complete penetrance
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
hematopoietic system phenotype
- 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)
- 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)
- anemia
- at E13.5, homozygotes are severely pale relative to wild-type embryos (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)
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
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
- 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)
- nervous system phenotype
- normal numbers of primary neurospheres are produced from cultured E10 telencephalic neuroepithelia (MGI Ref ID J:92520)
vision/eye phenotype
- vision/eye phenotype
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 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)
- 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)
behavior/neurological phenotype
- hunched posture
- at E13.5, 7 of 8 homozygotes display a hunchback posture (MGI Ref ID J:37145)
References
- 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: 1406933MGI: J:2511
Additional References
- 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: 8947040MGI: J:37025
- Novitch BG; Mulligan GJ; Jacks T; Lassar AB. 1996. Skeletal muscle cells lacking the retinoblastoma protein display defects in muscle gene expression and accumulate in S and G2 phases of the cell cycle. J Cell Biol 135(2):441-56. PubMed: 8896600MGI: J:36067
Additional - 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: 17956737MGI: 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: 20080939MGI: 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: 18599617MGI: 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: 17510234MGI: 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: 11246230MGI: 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: 19962666MGI: 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: 18299349MGI: 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: 8370518MGI: 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: 17173068MGI: 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: 17637742MGI: J:132091
- Cecchini MJ; Thwaites MJ; Talluri S; MacDonald JI; Passos DT; Chong JL; Cantalupo P; Stafford PM; Saenz-Robles MT; Francis SM; Pipas JM; Leone G; Welch I; Dick FA. 2014. A retinoblastoma allele that is mutated at its common E2F interaction site inhibits cell proliferation in gene-targeted mice. Mol Cell Biol 34(11):2029-45. PubMed: 24662053MGI: J:215358
- 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: 15919720MGI: 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: 18981426MGI: 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: 17975001MGI: J:127141
- Chinnam M; Wang X; Zhang X; Goodrich DW. 2016. Evaluating Effects of Hypomorphic Thoc1 Alleles on Embryonic Development in Rb1 Null Mice. Mol Cell Biol 36(11):1621-7. PubMed: 27001308MGI: J:236189
- 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: 16087217MGI: 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: 19015245MGI: 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: 20937698MGI: J:165519
- Clark AJ; Doyle KM; Humbert PO. 2004. Cell-intrinsic requirement for pRb in erythropoiesis. Blood 104(5):1324-6. PubMed: 15155463MGI: 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: 1406937MGI: 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: 22484813MGI: 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: 20551166MGI: 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: 9794240MGI: 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: 17822758MGI: 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: 15867358MGI: 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: 12732721MGI: 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: 17923680MGI: 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: 16809444MGI: J:113662
- Donangelo I; Melmed S. 2005. Pathophysiology of pituitary adenomas. J Endocrinol Invest 28(11 Suppl):100-5. PubMed: 16625857MGI: J:116408
- Donovan SL; Dyer MA. 2004. Developmental defects in Rb-deficient retinae. Vision Res 44(28):3323-33. PubMed: 15536000MGI: 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: 16672052MGI: 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: 13679855MGI: 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: 23474762MGI: 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: 19649275MGI: 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: 16912184MGI: 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: 11731416MGI: 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: 9751770MGI: 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: 9192872MGI: 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: 15616565MGI: J:95106
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