Ask about this productRelated genes to: SMARCC1 antibody
- Gene:
- SMARCC1 NIH gene
- Name:
- SWI/SNF related, matrix associated, actin dependent regulator of chromatin subfamily c member 1
- Previous symbol:
- -
- Synonyms:
- BAF155, SRG3, Rsc8, CRACC1
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1998-05-15
- Date modifiied:
- 2016-04-04
Related products to: SMARCC1 antibody
Related articles to: SMARCC1 antibody
- Liver progenitor-like cells (LPLCs) are essential for liver regeneration during some injury process, yet their epigenetic characters remain poorly understood. Using single-nucleus assay for transposase-accessible chromatin sequencing (snATAC-seq), we profiled chromatin accessibility in a mouse model of 3,5-diethoxycarbonyl-1,4-dihydrocollidin (DDC) diet-induced cholestasis at six time points: homeostasis (D0), injury (D8, D17), and repair (R2, R7, R21). We analyzed 75,452 high-quality nuclei, identifying 15 liver cell types, including LPLCs. Among 221,845 accessible chromatin regions, 192,079 showed differential accessibility. LPLCs exhibited enriched binding motifs for SWI/SNF (SMARCC1) and AP-1 (FOS, JUND and JUNB) complexes, highlighting their roles in transcriptional regulation. This study provides a comprehensive chromatin accessibility landscape of liver injury and regeneration, suggesting SWI/SNF and AP-1 as potential therapeutic targets. - Source: PubMed
Publication date: 2026/05/02
Wu HongYang YongqingWu YanXu JiangshanGuo PengchengLiu ShipingHou YongHao Shijie - Feeding behavior is a fundamental biological process closely linked to development, growth, metabolism, and immune regulation in animals. In livestock production, it serves as both an indicator of health status and a selection criterion for breeding programs aimed at improving feed efficiency and adaptive behavior. However, the genetic basis and regulatory mechanisms governing these traits remain poorly understood. In this study, we investigated the genomic architecture of feeding behavior in 205 slow-growing yellow broilers using whole-genome sequencing and high-resolution behavioral phenotyping recorded by automated feeders. Six feeding behavior traits - average daily feed intake, number of daily visits, daily feeding duration, feeding duration per visit, feed intake per visit, and feeding rate - along with 17 production traits in 205 slow-growing yellow broilers were analyzed. SNP-based heritability estimates ranged from 0.30 to 0.69, indicating moderate to high genetic control. Phenotypic and genetic correlations showed significant positive correlations with residual feed intake, suggesting their potential as breeding indicators of feed efficiency. Genome-wide association studies (GWAS) identified seven single nucleotide polymorphisms (SNPs) and three structural variants (SVs) significantly associated with time-related and intake-related feeding traits. Functional annotation and regulatory element prediction highlighted candidate genes, including SMARCC1, SLC15A2, SEMA5B, LRIG1, ARHGAP39, HSPBAP1, and MAPK15, which, based on public databases, were expressed across multiple tissues but showed relatively higher levels in neuro-related tissues, with the retina emerging as a common site of high expression. These genes are involved in chromatin remodeling, neuropeptide transport, retinal development, and stress response, supporting a potential regulatory role of the brain-retina axis in feeding behavior. Together, our findings identify candidate genomic loci and biological pathways associated with feeding behavior, providing new insights into the neural regulation of appetite and valuable molecular targets for genetic improvement of feed efficiency and animal welfare in poultry breeding. - Source: PubMed
Publication date: 2026/01/12
Wang PingZhai ShuangshuangZhao YangDai YuchiLi ChengxuanZheng YingyingMa ChunmeiYang NingYan Wei - Hepatocellular carcinoma is a devastating malignancy with numerous therapeutic targets to guide treatment strategies against the disease. However, given the limited efficacy of current frontline targeted therapies in prolonging the survival for HCC patients both as single agents and in combination, evaluating the potential of epigenome remodelling as a therapeutic target opens unexplored avenues for the clinical management of HCC. In this study, we identified epigenetic vulnerabilities to expand the repertoire of therapeutic strategies for HCC patients. To identify epigenetic regulators essential in HCC, we integrated the functional responses of six HCC cell lines to genetic perturbation of epigenetic regulators using esiRNA with existing data from publicly available databases. Correlation between phenotypic responses of HCC cells to large-scale genetic knockdown of epigenetic regulators and publicly available datasets narrowed down the pool of epigenetic vulnerabilities in HCC to two prospective epigenetic oncogenes (SUPT7L and SMARCC1) and one prospective epigenetic tumour suppressor (PHF2). Subsequently, PHF2 loss-of-function studies in HCC cells were performed through functional, molecular and proteomic analyses. Deeper investigations into PHF2 further established its functional role in mitigating cancer cell growth in vitro. Molecular and proteomic analyses in PHF2-deficient cells further suggested that PHF2 functionally suppresses cancer growth in part through the regulation of the cytoprotective protein, SRXN1. Further characterisation of PHF2-deficient cells were suggestive of independence from the Keap1-Nrf2 pathway. Collectively, our study suggests that PHF2 acts as a candidate epigenetic tumour suppressor in HCC patients through the downregulation of SRXN1, potentially independent of Nrf2. - Source: PubMed
Publication date: 2026/01/19
Thng Dexter Kai HaoHooi LissaYong Wai KhangKappei DennisToh Tan BoonChow Edward Kai-Hua - The c-MYC transcription factor is aberrantly expressed in most human cancers to enhance expression of proliferative gene programs. Owing to its pseudo-ordered structure and reliance on extensive and dynamic protein-protein interactions in distinct transcriptional regulatory complexes, defining context-specific MYC interactors has remained challenging. Therefore, mapping MYC-centered complex topologies in disease relevant models could identify components critical for its function which may serve as therapeutic targets in MYC-driven cancers. Here, we present a matched pair of photoproximity probes coupled with quantitative proteomics which enable context-dependent mapping of protein complex topology inside cells. We applied this spatially resolved, intracellular photoproximity (siPROX) profiling workflow to map MYC interactomes across temporal, spatial and disease-relevant contexts. Basal and inhibitor-treated profiles confirmed interactions with a wide range of known chromatin-associated transcriptional regulatory factors that define the extended MYC transcriptional bubble in live cells. Time-resolved mapping of inhibitor treated cells identified dynamic remodeling of numerous transcriptional regulatory factors and identified several BAF complex members (e.g., PBRM1 and SMARCC1) that persist in the presence of bromodomain inhibition. Furthermore, spatial MYC topology maps in small cell lung cancer cells confirmed the presence of BAF complex members under conditions where MYC induced target gene expression, altered cell morphology and enhanced proliferation. Lastly, loss of BAF function via inhibition of SMARCA2/4 ATPase activity resulted in rapid loss of chromatin-bound and nuclear MYC levels, downregulation of MYC-dependent transcripts and MYC-specific cell growth in several cancer cell models. Together, these data highlight the potential for siPROX to identify spatially resolved, dynamic TF interactors and highlight MYC-proximal BAF interactions as a targetable liability to regulate MYC-dependent transcription and proliferation. - Source: PubMed
Publication date: 2025/10/19
Carlos Anthony JHuang ShuyuanYang DongboSwenson ColinChakraborty PratyashaYu ShaopengStein Benjamin DMoellering Raymond E - The SWI/SNF complex is comprised of ATPase catalytic subunit SMARCA4/SMARCA2, evolutionarily conserved core subunits including SMARCB1, SMARCC1, and SMARCC2, as well as functionally specialized accessory subunits PBRM1 and ARID1A. Deletion or mutation of the catalytic subunit can lead to inactivation of the encoded protein and impaired overall function of the complex, contributing to tumorigenesis. - Source: PubMed
Publication date: 2025/09/12
Dai XiaominFeng XiaoyueLi JingPeng Fang