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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Transcriptional regulator, SIN3B

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Top mentioned proteins: mSin3A, Histone, CAN, HDAC, c-Myc
Papers on Sin3B
Transcriptional repression of Sin3B by Bmi-1 prevents cellular senescence and is relieved by oncogene activation.
David et al., New York City, United States. In Oncogene, Aug 2015
The expression of the chromatin-associated Sin3B protein is stimulated by oncogenic stress, and is required for oncogene-induced senescence.
pH might play a role in regulating the function of paired amphipathic helices domains of human Sin3B by altering structure and thermodynamic stability.
Singh et al., Delhi, India. In Biochemistry (mosc), Apr 2015
Human Sin3B (hSin3B), a transcription regulator, is a scaffold protein that binds to different transcription factors and regulates transcription.
Stress-mediated Sin3B activation leads to negative regulation of subset of p53 target genes.
Saluja et al., Delhi, India. In Biosci Rep, 2014
Previously, an increased expression of Sin3B and tumour suppressor protein, p53 has been established upon adriamycin treatment.
Physical and functional interactions between the histone H3K4 demethylase KDM5A and the nucleosome remodeling and deacetylase (NuRD) complex.
Nakayama et al., Kōbe, Japan. In J Biol Chem, 2014
Immunoaffinity purification of KDM5A confirmed a previously described association with the SIN3B-containing histone deacetylase complex and revealed an association with the nucleosome remodeling and deacetylase (NuRD) complex.
MYC through miR-17-92 suppresses specific target genes to maintain survival, autonomous proliferation, and a neoplastic state.
Felsher et al., Stanford, United States. In Cancer Cell, 2014
Here we report that MYC via miR-17-92 maintains a neoplastic state through the suppression of chromatin regulatory genes Sin3b, Hbp1, Suv420h1, and Btg1, as well as the apoptosis regulator Bim.
Sin3b interacts with Myc and decreases Myc levels.
Leon et al., Madrid, Spain. In J Biol Chem, 2014
A yeast two-hybrid screen has revealed that the transcriptional repressor Sin3b interacts with Myc protein.
Sin3B mediates collagen type I gene repression by interferon gamma in vascular smooth muscle cells.
Xu et al., Nanjing, China. In Biochem Biophys Res Commun, 2014
We show here that Sin3B, a component of the eukaryotic histone deacetylase (HDAC) complex, was recruited to COL1A2 transcription start site in response to IFN-γ treatment in VSMCs paralleling COL1A2 repression.
Senescence-associated SIN3B promotes inflammation and pancreatic cancer progression.
David et al., In J Clin Invest, 2014
We previously demonstrated that the histone deacetylase-associated protein SIN3B is essential for oncogene-induced senescence in cultured cells.
Interaction between the transcriptional corepressor Sin3B and voltage-gated sodium channels modulates functional channel expression.
Matthews et al., Los Reyes, Mexico. In Sci Rep, 2012
In this study, we identified the transcriptional regulator, Sin3B, as a novel binding partner of Na(v) channels in a yeast two-hybrid screen and confirmed the interaction using pull-down assays, co-immunoprecipitation, and immunofluorescence-colocalization.
Dissecting the complex regulation of Mad4 in glioblastoma multiforme cells.
Dorsey et al., Philadelphia, United States. In Cancer Biol Ther, 2012
Among proteins in the c-Myc/Max/Mad/Sin3 regulatory complex, Mad4 and Sin3B are routinely detected in human glioblastoma multiforme (GBM) cell lines.
Sin3 interacts with Foxk1 and regulates myogenic progenitors.
Garry et al., Minneapolis, United States. In Mol Cell Biochem, 2012
Sin3 has an important role in the regulation of cell cycle kinetics of the myogenic progenitor cell population
Paired tumor and normal whole genome sequencing of metastatic olfactory neuroblastoma.
Carpten et al., Scottsdale, United States. In Plos One, 2011
However, in the original surgical resection specimen (prior to evidence of metastatic disease), mutations in KDR, MYC, SIN3B, and NLRC4 genes were not present, suggesting that these were acquired with disease progression and/or as a result of post-treatment effects.
A novel mammalian complex containing Sin3B mitigates histone acetylation and RNA polymerase II progression within transcribed loci.
David et al., New York City, United States. In Mol Cell Biol, 2011
identification of a mammalian complex containing the corepressor Sin3B, the histone deacetylase HDAC1, Mrg15, and the PHD finger-containing Pf1
Tumor suppressor protein p53 recruits human Sin3B/HDAC1 complex for down-regulation of its target promoters in response to genotoxic stress.
Saluja et al., Delhi, India. In Plos One, 2010
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
The mammalian Sin3 proteins are required for muscle development and sarcomere specification.
Dynlacht et al., New York City, United States. In Mol Cell Biol, 2010
Results describe a novel transcriptional role for Sin3A and Sin3B proteins associated with maintenance of differentiated muscle cells.
Interference with Sin3 function induces epigenetic reprogramming and differentiation in breast cancer cells.
Waxman et al., New York City, United States. In Proc Natl Acad Sci U S A, 2010
disruption of the function of a specific Sin3A/B domain leads to epigenetic reprogramming and derepression of specific subsets of genes in breast cancer cells
Role for N-CoR and histone deacetylase in Sin3-mediated transcriptional repression.
DePinho et al., New York City, United States. In Nature, 1997
Mxi1-mediated inhibition of Myc activities requires interaction with mammalian Sin3A or Sin3B proteins, which have been purported to act as scaffolds for additional co-repressor factors.
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