Ask about this productRelated genes to: SIN3A antibody
- Gene:
- SIN3A NIH gene
- Name:
- SIN3 transcription regulator family member A
- Previous symbol:
- -
- Synonyms:
- KIAA0700, DKFZP434K2235
- Chromosome:
- 15q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-10-09
- Date modifiied:
- 2016-10-05
Related products to: SIN3A antibody
Related articles to: SIN3A antibody
- Histone Deacetylase (HDAC) 1 and 2 are key enzymatic components in multiple large chromatin remodeling complexes including NuRD, SIN3, and CoREST. In addition, both HDAC 1 and 2 contain a large intrinsically disordered region (IDR) within their C-terminal domain (CTD). How HDAC1/2 assemble into these complexes and the structure of the CTD IDR remains poorly understood. Here, we used HDAC1/2 to isolate their protein interaction networks from cells and used crosslinking mass spectrometry (XL-MS) coupled with the Integrative Modeling Platform to build structural models of the NuRD, SIN3A, and CoREST complexes. Next, we implemented an AlphaFold-enabled XL-MS constrained modeling approach to investigate how HDAC1 could assemble into these complexes. We show that the CTD IDR of HDAC1 folds into alpha helices in these complexes. Finally, we built a complete integrative structural model of a NuRD subcomplex including the abundant HDAC1:MBD3:MTA1:GATAD2B:RBBP4 subunits, which included 6 IDRs. The approaches used herein are broadly applicable for the study of protein complexes and protein interaction networks that can provide important insights into IDRs. - Source: PubMed
Publication date: 2026/09/01
Nde JulesMajila KartikZimmermann Rosalyn CKempf CassandraZhang YingCesare JosephThornton Janet LWorkman Jerry LFlorens LaurenceViswanath ShruthiWashburn Michael P - Fetal hemoglobin (Hb F) is the strongest endogenous modifier of sickle cell disease (SCD) severity, but its genetic regulation varies across populations. This review synthesized evidence on genetic determinants of Hb F and quantified effects of key variants through meta-analysis. Following PRISMA 2020 guidelines (PROSPERO: CRD420251042025), MEDLINE, EMBASE, Scopus, and Web of Science were searched through May 2026. Studies evaluating genetic associations with Hb F levels in SCD were included. Narrative synthesis and random-effects meta-analysis were performed. Eighty-four studies identified 80 variants across 32 genes associated with Hb F levels. The most consistently replicated associations involved (rs1427407, rs4671393, and rs11886868), the intergenic region (rs4895441, rs28384513), (rs7482144), and (rs2071746). Meta-analysis confirmed directionally consistent associations for seven of eight variants. Additional modifiers included , , , , , and . Hb F regulation in SCD is polygenic and influenced by both canonical and secondary modifiers, supporting genotype-guided therapeutic, and genome-editing strategies. - Source: PubMed
Publication date: 2026/08/17
Shende NandiniAthalye ShreyasiKamath SamriddhiRani PriyaMadkaikar ManishaBanerjee AninditaKhargekar Naveen - Triple-negative breast cancer (TNBC) remains a clinically challenging subtype characterized by aggressive behavior and limited treatment options. Though docetaxel remains a cornerstone chemotherapy for TNBC, the frequent emergence of resistance highlights the urgent need to identify novel therapeutic targets. In this study, we report that uncoordinated homeobox (UNCX) is upregulated in docetaxel-resistant breast cancer cells, genomically amplified in breast cancer, and associated with poor survival in breast carcinoma patients. Functional studies revealed that UNCX promotes breast cancer cell proliferation, migration and reduces the docetaxel sensitivity. Mechanistically, UNCX functions as a transcriptional repressor by recruiting the SIN3A complex. Genome-wide profiling indicated that the UNCX/SIN3A complex directly binds to the promoters of tumor-suppressor genes including FOXO3, and represses their transcription by removing histone H4K8 crotonylation (H4K8cr). Additionally, the UNCX/SIN3A complex enhances FOXO3 phosphorylation and inhibits its nuclear translocation, further inhibiting its activity. Notably, SIN3A knockdown, FOXO3 overexpression, or crotonylation restoration effectively reverses UNCX-induced malignant phenotypes. These findings collectively establish the UNCX/SIN3A-H4K8cr-FOXO3 axis as a pivotal epigenetic regulator of TNBC progression and chemoresistance, revealing new avenues for targeted therapeutic development against this aggressive breast cancer subtype. - Source: PubMed
Publication date: 2026/08/12
Shi SongfuYan DongZhao LixinZheng YihaoYe LingxiZeng YongjiaZeng LinghangWang FanWang WenjuanLiu Shumeng - Determining the recruitment relationships of nuclear proteins is essential for understanding the mechanisms underlying nuclear complex assembly and gene regulation. A widely used method for studying recruitment is chromatin immunoprecipitation (ChIP), but it requires fixation, chromatin shearing, and specific antibodies and cannot easily resolve recruitment directionality. Other systems like lacO/LacI are restricted to a limited number of specialized cell lines containing this lacO array's integration. To overcome these limitations, we developed a novel microscopy-based assay, CRISPR-PITA (protein interaction and telomere recruitment assay), to assess whether a nuclear protein can recruit other nuclear factors in living cells. The protein of interest is targeted to repetitive genomic loci (e.g., telomeres) using catalytically inactive Cas9 (dCas9) fused to a SunTag array, resulting in visible nuclear foci. Recruitment of endogenous proteins is evaluated by immunofluorescence. For proof-of-concept, we tested the Kaposi's sarcoma herpesvirus (KSHV) latency-associated nuclear antigen (LANA). CRISPR-PITA revealed that LANA recruits known interactors, such as ORC2 and SIN3A, but not MeCP2. Conversely, MeCP2 recruits LANA, indicating a unidirectional recruitment relationship. Similarly, MeCP2 could recruit HDAC1, while HDAC1 could not recruit MeCP2, further supporting directional nuclear interactions. Here, we present an easy, straightforward protocol applicable to any transfectable cell line, enabling researchers to dissect recruitment dynamics at high spatial resolution. CRISPR-PITA provides a powerful, flexible, and accessible platform to interrogate recruitment directionality between nuclear proteins in their native cellular context. Key features • Enables direct visualization of endogenous protein recruitment in living cells. • Detects directionality of recruitment. • Compatible with virtually any transfectable cell line. • Requires three days to complete. - Source: PubMed
Publication date: 2026/07/05
Lavi IdoBhattacharya SupriyaGurevich VyacheslavShamay Meir - The p47ING1a isoform of the ING1 tumor suppressor regulates cellular senescence through Rb-dependent pathways via its plant homeodomain (PHD) zinc-finger, which recognizes the H3K4me3 histone mark. However, the mutational landscape of p47ING1a and the functional consequences of PHD-domain nonsynonymous single-nucleotide polymorphisms (nsSNPs) remain poorly characterized. This study aimed to identify and structurally evaluate the most deleterious nsSNPs in p47ING1a and clarify their potential role in disrupting ING1 tumor-suppressor activity. - Source: PubMed
Rafi Md OliullahSarker Md TakimSheikh Mohammad AshikDas SowmitroHalder Sajal KumarIslam Md Ashiqul