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AML (show RUNX1 Proteins) patients with high SIN3 A expression levels had a worse prognosis than those with low expression. The same Y325Cvariant seen in endometrial carcinoma was found in one AML (show RUNX1 Proteins) patient. It was calculated to cause a predicted stability change of -1.433 Kcal/mol (show DUOXA1 Proteins), indicating significant disruption of the secondary structure.
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 (show THOC2 Proteins) interacts with the Sin3A histone deacetylase (show HDAC1 Proteins) 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 (show FOXN3 Proteins)-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 (show RUNX1 Proteins) and its partners SIN3A and TCF12 (show TCF12 Proteins) in myeloid leukemia (show BCL11A Proteins).
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 (show MLXIP Proteins)-202 increased the expression of its target Mxd1 (show MXD1 Proteins), followed by Mxd1 (show MXD1 Proteins) recruitment to the Sin3A repressor complex and through its dimerization with Max, and increased repression of Myc (show MYC Proteins)-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 (show MYC Proteins) with mSinA
Aberrantly expressed miR (show MLXIP Proteins)-210 regulates human U251 glioma cells apoptosis and proliferation partly through directly down-regulating SIN3A protein expression.
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 (show HDAC3 Proteins) complex in embryonic stem cells that is required to promote rapid proliferation and prevent unscheduled differentiation.
TGF-beta1 (show TGFB1 Proteins)-induced inhibition of PPARgamma (show PPARG Proteins) transcription depends on formation of a functional transcriptional regulatory complex that includes Smad3 (show SMAD3 Proteins), mSin3A and HDAC1 (show HDAC1 Proteins) at the PPARgamma (show PPARG Proteins) 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 (show HDAC1 Proteins)/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 (show AHR Proteins).
Treatment with GlcN, in contrast, inhibits LPS (show TLR4 Proteins)-ind inflammation and decreased LPS (show TLR4 Proteins)-mediated recruitment of OGT (show OGT Proteins), 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
, SIN3 transcription regulator homolog A
, histone deacetylase complex subunit Sin3a
, paired amphipathic helix protein Sin3a
, transcriptional co-repressor Sin3A
, transcriptional corepressor Sin3a
, transcriptional regulator, SIN3A
, transcriptional regulator, SIN3 yeast homolog A
, SIN3 homolog A, transcription regulator (yeast)
, paired amphipathic helix protein Sin3a-like
, SIN3 homolog A, transcription regulator a