ArticleGenes & development2000
Ablation of the retinoblastoma gene family deregulates G(1) control causing immortalization and increased cell turnover under growth-restricting conditions.
Article in Genes & development, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 199 papers.
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Who cites it
199 citing papers in PubMed.
- G0 or no-G0: phosphatase control of quiescence and cell cycle entry.Biochemical Society transactions · 2026Review
- Pin1 as a central node in oncogenic signaling: Mechanistic insights and clinical prospects (Review).Molecular medicine reports · 2025Review
- Derivation of human primary prostate epithelial cell lines by differentially targeting the CDKN2A locus along with expression of hTERT.Scientific reports · 2024Article
- APC/C prevents a noncanonical order of cyclin/CDK activity to maintain CDK4/6 inhibitor-induced arrest.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- HDAC activity is dispensable for repression of cell-cycle genes by DREAM and E2F:RB complexes.Nature communications · 2024Article
- Derivation of human primary prostate epithelial cell lines by differentially targeting theResearch square · 2024Article
- The pRb/RBL2-E2F1/4-GCN5 axis regulates cancer stem cell formation and G0 phase entry/exit by paracrine mechanisms.Nature communications · 2024Article
- APC/C prevents non-canonical order of cyclin/CDK activity to maintain CDK4/6 inhibitor-induced arrest.bioRxiv : the preprint server for biology · 2023Article
- HDAC activity is dispensable for repression of cell-cycle genes by DREAM and E2F:RB complexes.bioRxiv : the preprint server for biology · 2023Article
- RBL2-E2F-GCN5 guide cell fate decisions during tissue specification by regulating cell-cycle-dependent fluctuations of non-cell-autonomous signaling.Cell reports · 2023Article
- Monitoring the Cell Cycle of Tumor Cells in Mouse Models of Human Cancer.Cold Spring Harbor perspectives in medicine · 2023Article
- Significance of RB Loss in Unlocking Phenotypic Plasticity in Advanced Cancers.Molecular cancer research : MCR · 2023Article
- Retinoblastoma Protein Is Required for Epstein-Barr Virus Replication in Differentiated Epithelia.Journal of virology · 2023Article
- Emerging roles of i-motif in gene expression and disease treatment.Frontiers in pharmacology · 2023Review
- Expanding the prostate cancer cell line repertoire with ACRJ-PC28, an AR-negative neuroendocrine cell line derived from an African-Caribbean patient.Cancer research communications · 2022Article
- Increasing cell size remodels the proteome and promotes senescence.Molecular cell · 2022Article
- Simultaneous depletion of RB, RBL1 and RBL2 affects endoderm differentiation of human embryonic stem cells.PloS one · 2022Article
- Abrogation of Rb Tumor Suppression Initiates GBM in Differentiated Astrocytes by Driving a Progenitor Cell Program.Frontiers in oncology · 2022Article
- The cell cycle inhibitor RB is diluted in G1 and contributes to controlling cell size in the mouse liver.Frontiers in cell and developmental biology · 2022Article
- Tumor suppressor stars in yeast G1/S transition.Current genetics · 2021Review
139 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The retinoblastoma suppressor pRB belongs to the family of so-called pocket proteins, which also includes p107 and p130. These proteins may functionally overlap in cell cycle control and tumor suppression. We have generated an isogenic set of embryonic stem (ES) cell lines carrying single or compound loss-of-function mutations in the Rb gene family, including a cell line completely devoid of all three pocket proteins. None of the knockout combinations affected the growth characteristics of ES cells; however, concomitant ablation of all three pocket proteins strongly impaired their differentiation capacity. For the generated genotypes, primary mouse embryonic fibroblasts (MEFs) also were obtained. While inactivation of Rb alone did not alleviate the senescence response of MEFs, pRB/p107-deficient MEFs, after having adapted to in vitro culturing, continued to proliferate at modest rate. Additional ablation of p130 rendered MEFs completely insensitive to senescence-inducing signals and strongly increased their proliferation rate. Although triple-knockout MEFs retained anchorage dependence, they lacked proper G(1) control and showed increased cell turnover under growth-inhibiting conditions.
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