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High mRNA expression of SIN3A/low mRNA expression of SIN3B correlates with longer relapse free survival specifically in patients with triple negative breast cancer.
THO (zeige THOC2 Proteine) interacts with the Sin3A histone deacetylase (zeige HDAC1 Proteine) complex to suppress co-transcriptional R-loops, DNA damage, and replication impairment. Functional analyses show that histone hypo-acetylation prevents accumulation of harmful R-loops and RNA-mediated genomic instability.
the FOXN3 (zeige FOXN3 Proteine)-NEAT1-SIN3A complex promotes epithelial-to-mesenchymal transition and invasion of breast cancer cells in vitro as well as dissemination and metastasis of breast cancer in vivo
Haploinsufficiency of SIN3A causes mild intellectual disability by affecting the development of cortical integrity.
Two novel translocations leading to the inactivation of RUNX1 (zeige RUNX1 Proteine) and its partners SIN3A and TCF12 (zeige TCF12 Proteine) in myeloid leukemia (zeige BCL11A Proteine).
Study suggests a lack of association of SIN3A gene sequence variants with azoospermia caused by Sertoli cell-only syndrome in humans.
down regulation of miR (zeige MLXIP Proteine)-202 increased the expression of its target Mxd1 (zeige MXD1 Proteine), followed by Mxd1 (zeige MXD1 Proteine) recruitment to the Sin3A repressor complex and through its dimerization with Max, and increased repression of Myc (zeige MYC Proteine)-Max target proteins.
protein pairs significantly correlated with an increased risk of death in non-small cell lung cancer: mSin3A with p16, and c-Myc (zeige MYC Proteine) with mSinA
Aberrantly expressed miR (zeige MLXIP Proteine)-210 regulates human U251 glioma cells apoptosis and proliferation partly through directly down-regulating SIN3A protein expression.
Bone-marrow-specific deletion of Sin3a, indicated that Sin3a-associated HDAC1/2-activity is essential for hematopoietic stem cell homeostasis.
Members of the SIN3A/HDAC2 corepressor complex are enriched in an extended NANOG interactome.
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.
Taken together, Fam60a is an essential core subunit of a variant Sin3a-Hdac (zeige HDAC3 Proteine) complex in embryonic stem cells that is required to promote rapid proliferation and prevent unscheduled differentiation.
TGF-beta1 (zeige TGFB1 Proteine)-induced inhibition of PPARgamma (zeige PPARG Proteine) transcription depends on formation of a functional transcriptional regulatory complex that includes Smad3 (zeige SMAD3 Proteine), mSin3A and HDAC1 (zeige HDAC1 Proteine) at the PPARgamma (zeige PPARG Proteine) promoter.
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
Report role of myocardial mSin3A/HDAC1 (zeige HDAC1 Proteine)/2 complex in mediating the beneficial effects of exercise in diabetic cardiomyopathy.
SIN3A, generally regarded as a transcriptional repressor, is required for induction of gene transcription by the aryl hydrocarbon receptor (zeige AHR Proteine).
Treatment with GlcN, in contrast, inhibits LPS (zeige TLR4 Proteine)-ind inflammation and decreased LPS (zeige TLR4 Proteine)-mediated recruitment of OGT (zeige OGT Proteine), mSin3A, and HDACs.
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.
Sin3A-deleted testes exhibit a Sertoli-cell only phenotype, consistent with the absolute requirement for Sin3A in germ cells' development and/or viability.
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.
SIN3 homolog A, transcription regulator
, transcriptional co-repressor Sin3A
, paired amphipathic helix protein Sin3a
, SIN3 homolog A, transcription regulator (yeast)
, paired amphipathic helix protein Sin3a-like
, SIN3 transcription regulator homolog A
, histone deacetylase complex subunit Sin3a
, transcriptional corepressor Sin3a
, transcriptional regulator, SIN3A
, transcriptional regulator, SIN3 yeast homolog A