ArticleEMBO reports2007
BS69 is involved in cellular senescence through the p53-p21Cip1 pathway.
Article in EMBO reports, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
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- Novel intermolecular zinc fingers and redox-driven conformational changes dictate tumor suppressor ZMYND11's role in cooperative recognition of diverse targets.Nucleic acids research · 2026Article
- Systematic investigation of zinc finger MYND-type containing 11-mediated alternative splicing reveals notable events in prostate cancer.Asian journal of urology · 2026Article
- The protective effects of Agomelatine against Aβ1-42 oligomers-induced cellular senescence mediated by SIRT6 and Agomelatine's potential in AD treatment.Human cell · 2021Article
- Necdin modulates proliferative cell survival of human cells in response to radiation-induced genotoxic stress.BMC cancer · 2012Article
- Antagonistic TSC22D1 variants control BRAF(E600)-induced senescence.The EMBO journal · 2011Article
- The essence of senescence.Genes & development · 2010Review
- Drosophila SIN3 isoforms interact with distinct proteins and have unique biological functions.The Journal of biological chemistry · 2010Article
- Intrinsic structural disorder in adenovirus E1A: a viral molecular hub linking multiple diverse processes.Journal of virology · 2008Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The multidomain-containing cellular protein BS69 interacts with adenovirus E1A and several other viral and cellular factors, and acts as a transcription repressor. Here, we show that BS69 is involved in the p53-p21Cip1-mediated senescence pathway. Knockdown of BS69 by RNA interference in human primary fibroblasts results in elevated levels of p21Cip1 and the appearance of several senescent markers, including enhanced senescence-associated beta-galactosidase activity and formation of senescence-associated heterochromatin foci. Importantly, knockdown of either p53 or p21Cip1, but not p16(INK4a) or Rb, allows cells to bypass premature senescence that is induced by BS69 knockdown. Furthermore, we show that BS69 forms complexes with both p53 and p400, and that BS69 associates with the p21Cip1 promoter through p53. Together, our data indicate that BS69 is involved in cellular senescence mainly through the p53-p21Cip1 pathway.
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Registered trials
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.