ArticlePloS one2011
Tumor suppressor protein p53 recruits human Sin3B/HDAC1 complex for down-regulation of its target promoters in response to genotoxic stress.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 40 citations in OpenAlex.
- Harnessing p53 for targeted cancer therapy: new advances and future directions.Transcription · 2025Review
- Switch-Independent 3A: An Epigenetic Regulator in Cancer with New Implications for Pulmonary Arterial Hypertension.Biomedicines · 2023Review
- Isoforms of the transcriptional cofactor SIN3 differentially regulate genes necessary for energy metabolism and cell survival.Biochimica et biophysica acta. Molecular cell research · 2022Article
- Mitotic and DNA Damage Response Proteins: Maintaining the Genome Stability and Working for the Common Good.Frontiers in cell and developmental biology · 2021Review
- Activation of farnesoid X receptor (FXR) induces crystallin zeta expression in mouse medullary collecting duct cells.Pflugers Archiv : European journal of physiology · 2020Article
- Zeta-crystallin: a moonlighting player in cancer.Cellular and molecular life sciences : CMLS · 2020Review
- IFIT1 Exerts Opposing Regulatory Effects on the Inflammatory and Interferon Gene Programs in LPS-Activated Human Macrophages.Cell reports · 2018Article
- Zebrafish sin3b mutants are viable but have size, skeletal, and locomotor defects.Developmental dynamics : an official publication of the American Association of Anatomists · 2017Article
- Census and evaluation of p53 target genes.Oncogene · 2017Review
- Molecular genetic response to varied wavelengths of light in Xiphophorus maculatus skin.Comparative biochemistry and physiology. Toxicology & pharmacology : CBP · 2015Article
- Article
- Magnolol inhibits growth of gallbladder cancer cells through the p53 pathway.Cancer science · 2015Article
- Stress-mediated Sin3B activation leads to negative regulation of subset of p53 target genes.Bioscience reports · 2015Article
- Article
- The transcription factor p53: not a repressor, solely an activator.Cell cycle (Georgetown, Tex.) · 2014Article
- The Justy mutant mouse strain produces a spontaneous murine model of salivary gland cancer with myoepithelial and basal cell differentiation.Laboratory investigation; a journal of technical methods and pathology · 2013Article
- Expression level of histone deacetylase 2 correlates with occurring of chronic obstructive pulmonary diseases.Molecular biology reports · 2013Article
- Phospho-ΔNp63α/microRNA feedback regulation in squamous carcinoma cells upon cisplatin exposure.Cell cycle (Georgetown, Tex.) · 2013Article
- Epigenetic regulation of gene expression in keratinocytes.The Journal of investigative dermatology · 2012Review
- Proteomic analysis of the nuclear phosphorylated proteins in dairy cow mammary epithelial cells treated with estrogen.In vitro cellular & developmental biology. Animal · 2012Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Master regulator protein p53, popularly known as the "guardian of genome" is the hub for regulation of diverse cellular pathways. Depending on the cell type and severity of DNA damage, p53 protein mediates cell cycle arrest or apoptosis, besides activating DNA repair, which is apparently achieved by regulation of its target genes, as well as direct interaction with other proteins. p53 is known to repress target genes via multiple mechanisms one of which is via recruitment of chromatin remodelling Sin3/HDAC1/2 complex. Sin3 proteins (Sin3A and Sin3B) regulate gene expression at the chromatin-level by serving as an anchor onto which the core Sin3/HDAC complex is assembled. The Sin3/HDAC co-repressor complex can be recruited by a large number of DNA-binding transcription factors. Sin3A has been closely linked to p53 while Sin3B is considered to be a close associate of E2Fs. The theme of this study was to establish the role of Sin3B in p53-mediated gene repression. We demonstrate a direct protein-protein interaction between human p53 and Sin3B (hSin3B). Amino acids 1-399 of hSin3B protein are involved in its interaction with N-terminal region (amino acids 1-108) of p53. Genotoxic stress induced by Adriamycin treatment increases the levels of hSin3B that is recruited to the promoters of p53-target genes (HSPA8, MAD1 and CRYZ). More importantly recruitment of hSin3B and repression of the three p53-target promoters upon Adriamycin treatment were observed only in p53(+/+) cell lines. Additionally an increased tri-methylation of the H3K9 residue at the promoters of HSPA8 and CRYZ was also observed following Adriamycin treatment. The present study highlights for the first time the essential role of Sin3B as an important associate of p53 in mediating the cellular responses to stress and in the transcriptional repression of genes encoding for heat shock proteins or proteins involved in regulation of cell cycle and apoptosis.
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