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

Transcriptional regulator, SIN3A

mSin3A, Sin3A, Sin3
The protein encoded by this gene is a transcriptional regulatory protein. It contains paired amphipathic helix (PAH) domains, which are important for protein-protein interactions and may mediate repression by the Mad-Max complex. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Histone, HDAC, CAN, CYP3A4, V1a
Papers on mSin3A
Regulation of neural gene transcription by optogenetic inhibition of the RE1-silencing transcription factor.
Benfenati et al., Genova, Italy. In Proc Natl Acad Sci U S A, Feb 2016
To tune REST activity, we selected two protein domains that impair REST-DNA binding or recruitment of the cofactor mSin3a.
MSI1 functions in a HDAC complex to fine-tune ABA signaling.
Hennig et al., Uppsala, Sweden. In Plant Cell, Jan 2016
We co-purified histone deacetylase 19 (HDA19) with MSI1 and SIN3-like proteins and provide evidence that MSI1 and HDA19 associate into the same complex in vivo.
Evidence for a non-canonical role of HDAC5 in regulation of the cardiac Ncx1 and Bnp genes.
Menick et al., United States. In Nucleic Acids Res, Jan 2016
Using the HDAC5((-/-)) mouse we show that HDAC5 is required for the interaction of the HDAC1/2/Sin3a co-repressor complexes with the Nkx2.5 and YY1 transcription factors and critical for recruitment of the HDAC1/Sin3a co-repressor complex to either the Ncx1 or Bnp promoter.
Long Noncoding RNA FosDT Promotes Ischemic Brain Injury by Interacting with REST-Associated Chromatin-Modifying Proteins.
Vemuganti et al., Madison, United States. In J Neurosci, Jan 2016
Focal ischemia also increased FosDT binding to chromatin-modifying proteins (CMPs) Sin3a and coREST (corepressors of the transcription factor REST).
The Molybdenum(V) and Tungsten(VI) Oxoazides [MoO(N3 )3 ], [MoO(N3 )3 ⋅2 CH3 CN], [(bipy)MoO(N3 )3 ], [MoO(N3 )5 ](2-) , [WO(N3 )4 ], and [WO(N3 )4 ⋅CH3 CN].
Christe et al., Los Angeles, United States. In Angew Chem Int Ed Engl, Jan 2016
A series of novel molybdenum(V) and tungsten(VI) oxoazides was prepared starting from [MOF4 ] (M=Mo, W) and Me3 SiN3 .
The role of TRIB1 in lipid metabolism; from genetics to pathways.
Nakayama et al., Tochigi, Japan. In Biochem Soc Trans, Nov 2015
Furthermore, novel binding partner, Sin3A (Swi-independent 3A)-associated protein, 18 kDa, was identified, which activates microsomal TG transfer protein (MTTP) expression by binding with MTTP regulatory elements in co-ordination with mSin3A and TRIB1.
Orphan nuclear receptor NR4A1 regulates transforming growth factor-β signaling and fibrosis.
Distler et al., Erlangen, Germany. In Nat Med, Feb 2015
NR4A1 recruits a repressor complex comprising SP1, SIN3A, CoREST, LSD1, and HDAC1 to TGF-β target genes, thereby limiting pro-fibrotic TGF-β effects.
Foxk proteins repress the initiation of starvation-induced atrophy and autophagy programs.
Dynlacht et al., New York City, United States. In Nat Cell Biol, 2014
Foxk1/2 specifically recruits Sin3A-HDAC complexes to restrict acetylation of histone H4 and expression of critical autophagy genes.
TET proteins and epigenetic modifications in cancers.
Krześlak et al., Łódź, Poland. In Postepy Hig Med Dosw (online), 2014
EZH2, OGT, Sin3a or HCF1) and by affecting their activity and, chromatin binding ability, they can cause changes in patterns of histone methylation, acetylation and O-GlcNAcylation.
The potential role of O-GlcNAc modification in cancer epigenetics.
Krześlak et al., Łódź, Poland. In Cell Mol Biol Lett, 2014
OGT can link the cellular metabolic state and the epigenetic status of cancer cells by interacting with and modifying many epigenetic factors, such as HCF-1, TET, mSin3A, HDAC, and BAP1.
MeCP2 phosphorylation in the brain: from transcription to behavior.
Heumann et al., In Biol Chem, 2013
In association with the transcriptional corepressor proteins Sin3a and histone deacetylases, it represses gene transcription.
p27(Kip1) directly represses Sox2 during embryonic stem cell differentiation.
Serrano et al., Madrid, Spain. In Cell Stem Cell, 2013
Mechanistically, we have found that upon differentiation p27 associates to the SRR2 enhancer of the Sox2 gene together with a p130-E2F4-SIN3A repressive complex.
Metastasis suppression by BRMS1 associated with SIN3 chromatin remodeling complexes.
Hurst, Birmingham, United States. In Cancer Metastasis Rev, 2012
Breast cancer metastasis suppressor 1 (BRMS1) interacts with SIN3 chromatin remodeling complexes, and, upon forced expression in metastatic cells, a nearly complete suppression of metastasis is noted without preventing primary tumor growth.
Chromatin associated Sin3A is essential for male germ cell lineage in the mouse.
David et al., New York City, United States. In Dev Biol, 2012
Sin3A-deleted testes exhibit a Sertoli-cell only phenotype, consistent with the absolute requirement for Sin3A in germ cells' development and/or viability.
The Sin3a repressor complex is a master regulator of STAT transcriptional activity.
Tavernier et al., Gent, Belgium. In Proc Natl Acad Sci U S A, 2012
The Sin3a complex acts as a context-dependent ISGF3/STAT3 transcriptional switch.
Ume6 transcription factor is part of a signaling cascade that regulates autophagy.
Klionsky et al., Ann Arbor, United States. In Proc Natl Acad Sci U S A, 2012
Ume6 is a negative regulator of ATG8 transcription, which acts along with a histone deacetylase complex including Sin3 and Rpd3 to regulate Atg8 levels
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
Allelic variation and differential expression of the mSIN3A histone deacetylase complex gene Arid4b promote mammary tumor growth and metastasis.
Hunter et al., Bethesda, United States. In Plos Genet, 2012
ARID4B physically interacts with the breast cancer metastasis suppressor BRMS1, and we detected differential binding of the Arid4b alleles to mSIN3A and mSDS3
The opposing transcriptional functions of Sin3a and c-Myc are required to maintain tissue homeostasis.
Frye et al., Cambridge, United Kingdom. In Nat Cell Biol, 2011
Sin3a causes deacetylation of c-Myc protein to directly repress c-Myc activity.
A molecular mechanism for circadian clock negative feedback.
Weitz et al., Boston, United States. In Science, 2011
analysis indicates PSF within the PER complex recruits SIN3A, a scaffold for assembly of transcriptional inhibitory complexes, and the PER complex thereby rhythmically delivers histone deacetylases to the Per1 promoter, which repress Per1 transcription
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