ArticleOncogene2015
Transcriptional repression of Sin3B by Bmi-1 prevents cellular senescence and is relieved by oncogene activation.
Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- miR-96-5p expression is sufficient to induce and maintain the senescent cell fate in the absence of stress.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Chromatin accessibility and cell cycle progression are controlled by the HDAC-associated Sin3B protein in murine hematopoietic stem cells.Epigenetics & chromatin · 2024Article
- Correlations between C-myc expression, BMI-1 expression, and vaginal microecology with HPV-DNA load in patients with different cervical lesions.American journal of translational research · 2024Article
- Quercetin Prevents Radiation-Induced Oral Mucositis by Upregulating BMI-1.Oxidative medicine and cellular longevity · 2021Article
- Review
- The HDAC-Associated Sin3B Protein Represses DREAM Complex Targets and Cooperates with APC/C to Promote Quiescence.Cell reports · 2018Article
- Chromatin-Associated Protein SIN3B Prevents Prostate Cancer Progression by Inducing Senescence.Cancer research · 2017Article
- Upregulation of the proto-oncogene Bmi-1 predicts a poor prognosis in pediatric acute lymphoblastic leukemia.BMC cancer · 2017Article
- The chromatin-associated Sin3B protein is required for hematopoietic stem cell functions in mice.Blood · 2017Article
- Bmi-1: At the crossroads of physiological and pathological biology.Genes & diseases · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The Polycomb group protein Bmi-1 is an essential regulator of cellular senescence and is believed to function largely through the direct repression of the Ink4a/Arf locus. However, concurrent deletion of Ink4a/Arf does not fully rescue the defects detected in Bmi-1(-/-) mice, indicating that additional Bmi-1 targets remain to be identified. The expression of the chromatin-associated Sin3B protein is stimulated by oncogenic stress, and is required for oncogene-induced senescence. Here we demonstrate that oncogenic stress leads to the dissociation of Bmi-1 from the Sin3B locus, resulting in increased Sin3B expression and subsequent entry into cellular senescence. Furthermore, Sin3B is required for the senescent phenotype and elevated levels of reactive oxygen species elicited upon Bmi-1 depletion. Altogether, these results identify Sin3B as a novel direct target of Bmi-1, and establish Bmi-1-driven repression of Sin3B as an essential regulator of cellular senescence.
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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.