ArticleOncogene2009
Rb2/p130 is the dominating pocket protein in the p53-p21 DNA damage response pathway leading to senescence.
Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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Who cites it
33 citing papers in PubMed, 59 citations in OpenAlex.
- E6AP is essential for the proliferation of HPV-positive cancer cells by preventing senescence.PLoS pathogens · 2025Article
- Unraveling the Guardian: p53's Multifaceted Role in the DNA Damage Response and Tumor Treatment Strategies.International journal of molecular sciences · 2024Review
- p15Heliyon · 2023Article
- AKTIP loss is enriched in ERα-positive breast cancer for tumorigenesis and confers endocrine resistance.Cell reports · 2022Article
- Article
- Cellular Senescence: Molecular Targets, Biomarkers, and Senolytic Drugs.International journal of molecular sciences · 2022Review
- FZD5 regulates cellular senescence in human mesenchymal stem/stromal cells.Stem cells (Dayton, Ohio) · 2021Article
- Role of p53 in the Regulation of Cellular Senescence.Biomolecules · 2020Review
- DREAM and RB cooperate to induce gene repression and cell-cycle arrest in response to p53 activation.Nucleic acids research · 2019Article
- Blockage of glutamine-dependent anaplerosis affects mTORC1/2 activity and ultimately leads to cellular senescence-like response.Biology open · 2019Article
- Article
- Misidentified Human Gene Functions with Mouse Models: The Case of the Retinoblastoma Gene Family in Senescence.Neoplasia (New York, N.Y.) · 2017Article
- Senoptosis: non-lethal DNA cleavage as a route to deep senescence.Oncotarget · 2017Article
- The cell fate: senescence or quiescence.Molecular biology reports · 2016Review
- To senesce or not to senesce: how primary human fibroblasts decide their cell fate after DNA damage.Aging · 2016Article
- Proteomic analysis reveals a role for Bcl2-associated athanogene 3 and major vault protein in resistance to apoptosis in senescent cells by regulating ERK1/2 activation.Molecular & cellular proteomics : MCP · 2015Article
- p53-dependent gene repression through p21 is mediated by recruitment of E2F4 repression complexes.Oncogene · 2014Article
- Cell senescence in myxoid/round cell liposarcoma.Sarcoma · 2014Article
- Ninjurin1, a target of p53, regulates p53 expression and p53-dependent cell survival, senescence, and radiation-induced mortality.Proceedings of the National Academy of Sciences of the United States of America · 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
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The different pocket proteins are established as negative cell cycle regulators. With regard to the repressor functions of pocket proteins in cellular senescence, studies so far have mainly focused on pRb/p105. Here, we show that in a broad range of wild-type p53-expressing human tumor cells, and in human diploid fibroblasts, Rb2/p130 is the dominating pocket protein in replicative and in accelerated senescence. Senescent cells are arrested at the transition from late G1- to early S-phase, as indicated by the absence of S- and G2-phase cyclins A and B. Expression of cyclin A and entry into S-phase resumed after RNA interference-mediated knockdown of Rb2/p130. Activation of different upstream pathways by overexpression of either p21 or p16 converged on Rb2/p130 accumulation and induced senescence. In contrast, p53- or p21-negative cells treated with DNA-damaging agents failed to accumulate Rb2/p130 and to enter senescence. Our data suggest that Rb2/p130 is a member of the p53-p21 DNA damage signaling cascade, and represents the essential pocket protein family member needed for the induction of any type of senescence.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.