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Members of the SIN3A/HDAC2 corepressor complex are enriched in an extended NANOG interactome.
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The co-repressor protein Sin3a is crucial for lung endoderm development. Loss of Sin3a in early foregut endoderm led to a specific and profound defect in lung development with lung buds failing to undergo branching morphogenesis and progressive atrophy of the proximal lung endoderm with complete epithelial loss at later stages of development.
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Taken together, Fam60a is an essential core subunit of a variant Sin3a-Hdac complex in embryonic stem cells that is required to promote rapid proliferation and prevent unscheduled differentiation.
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TGF-beta1-induced inhibition of PPARgamma transcription depends on formation of a functional transcriptional regulatory complex that includes Smad3, mSin3A and HDAC1 at the PPARgamma promoter.
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Sin3a mRNA is recruited during maturation and that inhibiting its recruitment not only inhibits development beyond the 2-cell stage but also compromises the fidelity of reprogramming gene expression
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Report role of myocardial mSin3A/HDAC1/2 complex in mediating the beneficial effects of exercise in diabetic cardiomyopathy.
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SIN3A, generally regarded as a transcriptional repressor, is required for induction of gene transcription by the aryl hydrocarbon receptor.
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As a result of differences in the components and targets of the Rest complex, its functional roles may differ in embryonic stem cells and epiblast stem cells.
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Treatment with GlcN, in contrast, inhibits LPS-ind inflammation and decreased LPS-mediated recruitment of OGT, mSin3A, and HDACs.
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Within the male germline, Sin3a is required for the mitotic reentry of gonocytes, but is dispensable for the maintenance of differentiating spermatogonia and subsequent spermatogenic processes.
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Sin3A-deleted testes exhibit a Sertoli-cell only phenotype, consistent with the absolute requirement for Sin3A in germ cells' development and/or viability.
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Sin3 has an important role in the regulation of cell cycle kinetics of the myogenic progenitor cell population
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ARID4B physically interacts with the breast cancer metastasis suppressor BRMS1, and we detected differential binding of the Arid4b alleles to mSIN3A and mSDS3
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Results indicate that Sin3a protects the genomic integrity of pluripotent embryonic cells and governs their unusual cell cycle.
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Sin3a causes deacetylation of c-Myc protein to directly repress c-Myc activity.
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show using NMR that the mSin3A PAH3-SAP30 SID complex can bind to nucleic acids, hinting at a role for a nucleolar localization sequence in the SID alphaA helix in targeting the Rpd3L/Sin3L complex for silencing ribosomal RNA genes
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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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Sin3a is required by sertoli cells to establish a niche for undifferentiated spermatogonia, germ cell tumors, and spermatid elongation.
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Results describe a novel transcriptional role for Sin3A and Sin3B proteins associated with maintenance of differentiated muscle cells.
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ESET histone methyltransferase can form a large, multi-protein complex(es) with mSin3A/B co-repressors and HDAC1/2 that participates in multiple pathways of transcriptional repression.
