ArticleMolecular and cellular biology2003
Conditional mutation of Rb causes cell cycle defects without apoptosis in the central nervous system.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 142 citations in OpenAlex.
- Pyruvate kinase M2 in Alzheimer's disease: from dysregulation to therapeutic inhibition.Brain communications · 2026Review
- Gremlin-2 is a novel tumor suppressor that negatively regulates ID1 in breast cancer.Breast cancer research : BCR · 2024Article
- Role of RB1 in neurodegenerative diseases: inhibition of post-mitotic neuronal apoptosis via Kmt5b.Cell death discovery · 2024Article
- SARS-CoV-2 Exacerbates Beta-Amyloid Neurotoxicity, Inflammation and Oxidative Stress in Alzheimer's Disease Patients.International journal of molecular sciences · 2021Article
- Stepwise crosstalk between aberrant Nf1, Tp53 and Rb signalling pathways induces gliomagenesis in zebrafish.Brain : a journal of neurology · 2021Article
- Cell Cycle Re-entry in the Nervous System: From Polyploidy to Neurodegeneration.Frontiers in cell and developmental biology · 2021Review
- Article
- Cell Cycle Proteins as Key Regulators of Postmitotic Cell Death.The Yale journal of biology and medicine · 2019Review
- Misidentified Human Gene Functions with Mouse Models: The Case of the Retinoblastoma Gene Family in Senescence.Neoplasia (New York, N.Y.) · 2017Article
- Retinoblastoma protein controls growth, survival and neuronal migration in human cerebral organoids.Development (Cambridge, England) · 2017Article
- Deletions of Retinoblastoma 1 (Rb1) and Its Repressing Target S Phase Kinase-associated protein 2 (Skp2) Are Synthetic Lethal in Mouse Embryogenesis.The Journal of biological chemistry · 2016Article
- Biomaterial-engineering and neurobiological approaches for regenerating the injured cerebral cortex.Regenerative therapy · 2016Review
- Increased mitochondrial function downstream from KDM5A histone demethylase rescues differentiation in pRB-deficient cells.Genes & development · 2015Article
- Transcriptional control of stem cell fate by E2Fs and pocket proteins.Frontiers in genetics · 2015Review
- Silencing of RB1 and RB2/P130 during adipogenesis of bone marrow stromal cells results in dysregulated differentiation.Cell cycle (Georgetown, Tex.) · 2014Article
- Article
- Loss of pRB and p107 disrupts cartilage development and promotes enchondroma formation.Oncogene · 2013Article
- Elevated Id2 expression results in precocious neural stem cell depletion and abnormal brain development.Stem cells (Dayton, Ohio) · 2013Article
- Silencing of RB1 but not of RB2/P130 induces cellular senescence and impairs the differentiation potential of human mesenchymal stem cells.Cellular and molecular life sciences : CMLS · 2013Article
- The retinoblastoma protein is essential for survival of postmitotic neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Targeted disruption of the retinoblastoma gene in mice leads to embryonic lethality in midgestation accompanied by defective erythropoiesis. Rb(-/-) embryos also exhibit inappropriate cell cycle activity and apoptosis in the central nervous system (CNS), peripheral nervous system (PNS), and ocular lens. Loss of p53 can prevent the apoptosis in the CNS and lens; however, the specific signals leading to p53 activation have not been determined. Here we test the hypothesis that hypoxia caused by defective erythropoiesis in Rb-null embryos contributes to p53-dependent apoptosis. We show evidence of hypoxia in CNS tissue from Rb(-/-) embryos. The Cre-loxP system was then used to generate embryos in which Rb was deleted in the CNS, PNS and lens, in the presence of normal erythropoiesis. In contrast to the massive CNS apoptosis in Rb-null embryos at embryonic day 13.5 (E13.5), conditional mutants did not have elevated apoptosis in this tissue. There was still significant apoptosis in the PNS and lens, however. Rb(-/-) cells in the CNS, PNS, and lens underwent inappropriate S-phase entry in the conditional mutants at E13.5. By E18.5, conditional mutants had increased brain size and weight as well as defects in skeletal muscle development. These data support a model in which hypoxia is a necessary cofactor in the death of CNS neurons in the developing Rb mutant embryo.
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