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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.
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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.
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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.
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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
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Haploinsufficiency of SIN3A causes mild intellectual disability by affecting the development of cortical integrity.
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Two novel translocations leading to the inactivation of RUNX1 and its partners SIN3A and TCF12 in myeloid leukemia.
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Study suggests a lack of association of SIN3A gene sequence variants with azoospermia caused by Sertoli cell-only syndrome in humans.
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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.
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protein pairs significantly correlated with an increased risk of death in non-small cell lung cancer: mSin3A with p16, and c-Myc with mSinA
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Aberrantly expressed miR-210 regulates human U251 glioma cells apoptosis and proliferation partly through directly down-regulating SIN3A protein expression.
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Bone-marrow-specific deletion of Sin3a, indicated that Sin3a-associated HDAC1/2-activity is essential for hematopoietic stem cell homeostasis.
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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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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
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BIM silencing in anaplastic large cell lymphoma occurs through recruitment of MeCP2 and the SIN3a/histone deacetylase 1/2 corepressor complex.
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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
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The Sin3a complex acts as a context-dependent ISGF3/STAT3 transcriptional switch.
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Ume6 is a negative regulator of ATG8 transcription, which acts along with a histone deacetylase complex including Sin3 and Rpd3 to regulate Atg8 levels
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Interplay between SIN3A and STAT3 mediates chromatin conformational changes and GFAP expression during cellular differentiation.(
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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.
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The study identifies Sin3A as a regulator of gene expression, survival, and growth in ERalpha-positive breast cancer cells.
