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SINHCAF/FAM60A and SIN3A specifically repress HIF-2alpha expression.
AML 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 patient. It was calculated to cause a predicted stability change of -1.433 Kcal/mol, 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 interacts with the Sin3A histone deacetylase 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-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 and its partners SIN3A and TCF12 in myeloid leukemia.
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-202 increased the expression of its target Mxd1, followed by Mxd1 recruitment to the Sin3A repressor complex and through its dimerization with Max, and increased repression of Myc-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 with mSinA
Aberrantly expressed miR-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.
SIN3A, generally regarded as a transcriptional repressor, is required for induction of gene transcription by the aryl hydrocarbon receptor.
EBNA3C binds strongly to BATF/IRF4/SPI1/RUNX3 sites to enhance transcription and recruits RBPJ/Sin3A- and REST/NRSF-repressive complexes to repress p14(ARF) and p16(INK4A) expression
BIM silencing in anaplastic large cell lymphoma occurs through recruitment of MeCP2 and the SIN3a/histone deacetylase 1/2 corepressor complex.
reducing Sin3A strongly increased the invasive behavior of A549 human lung adenocarcinoma cells; findings show that Sin3A is downregulated in a variety of human tumors
The Sin3a complex acts as a context-dependent ISGF3/STAT3 transcriptional switch.
Ume6 is a negative regulator of ATG8 transcription, which acts along with a histone deacetylase complex including Sin3 and Rpd3 to regulate Atg8 levels
Interplay between SIN3A and STAT3 mediates chromatin conformational changes and GFAP expression during cellular differentiation.(
Sin3a, HDAC1, and YY1 are co-factors for Gon4l and that Gon4l may function as a platform for the assembly of complexes that regulate gene 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 complex in embryonic stem cells that is required to promote rapid proliferation and prevent unscheduled differentiation.
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.
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/HDAC1/2 complex in mediating the beneficial effects of exercise in diabetic cardiomyopathy.
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.
Treatment with GlcN, in contrast, inhibits LPS-ind inflammation and decreased LPS-mediated recruitment of OGT, 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.
Sin3 has an important role in the regulation of cell cycle kinetics of the myogenic progenitor cell population
ARID4B physically interacts with the breast cancer metastasis suppressor BRMS1, and we detected differential binding of the Arid4b alleles to mSIN3A and mSDS3
Results indicate that Sin3a protects the genomic integrity of pluripotent embryonic cells and governs their unusual cell cycle.
Sin3a causes deacetylation of c-Myc protein to directly repress c-Myc activity.
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
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
Sin3a is required by sertoli cells to establish a niche for undifferentiated spermatogonia, germ cell tumors, and spermatid elongation.
Results describe a novel transcriptional role for Sin3A and Sin3B proteins associated with maintenance of differentiated muscle cells.
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.
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