Ask about this productRelated genes to: SMARCD3 antibody
- Gene:
- SMARCD3 NIH gene
- Name:
- SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily d, member 3
- Previous symbol:
- -
- Synonyms:
- BAF60C, Rsc6p, CRACD3
- Chromosome:
- 7q36.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-05-15
- Date modifiied:
- 2016-10-05
Related products to: SMARCD3 antibody
Related articles to: SMARCD3 antibody
- Malignant Peripheral Nerve Sheath Tumors (MPNSTs) are aggressive sarcomas of peripheral nerve sheath that frequently arise in patients with neurofibromatosis type 1 (NF1) and currently have no approved targeted treatment. Loss of Polycomb Repressive Complex 2 (PRC2) activity, through inactivating mutations in SUZ12 or EED, occurs in 50 to 80% of NF1-associated MPNSTs, leads to depletion of H3K27me3 in cells, global epigenetic dysregulation, and serves as an indicator of poor clinical outcomes. SWI/SNF (BAF) complexes are ATPase-driven chromatin remodelers essential for orderly transcriptional activity in cells. Because PRC2 and SWI/SNF enforce functionally antagonistic effects on chromatin, we hypothesized that PRC2-deficient MPNSTs undergo alterations in the SWI/SNF complex that create a therapeutic vulnerability to SWI/SNF inhibition. We performed integrated proteogenomic profiling of patient-derived MPNST cell lines stratified by PRC2 status: Loss of Function (LoF) or Wild Type (WT). We found that PRC2 loss in MPNST was associated with broad reduction in global SWI/SNF protein abundance, recurrent enrichment of SMARCD3 in SMARCA4-containing complexes, and context-dependent enrichment of DPF3 and PBAF-specific subunits. ChIP-seq analyses showed redistribution of cBAF and PBAF chromatin occupancy in PRC2 LoF models followed by concordant increases in H3K27ac signal and gene expression. Cell fitness assays revealed that the SWI/SNF ATPase inhibitor, FHD-286, reduced cell viability in PRC2 LoF MPNST lines at low nanomolar concentrations and disrupted the colony forming ability, while PRC2 WT cell lines were less sensitive to treatment. Finally, evaluating the efficacy of FHD-286 alone, and in combination with I-BET-762, in an isogenic PRC2 loss murine allograft MPNST model, we observed enhanced efficacy of the combination regimen compared to either single agent in the Suz12 KO arm, while in the Suz12 WT arm, the combo was outperformed by I-BET-762 alone. Together, our findings indicate that PRC2 loss in MPNST is accompanied by selective subunit remodeling and genomic redistribution of SWI/SNF complexes and support SWI/SNF ATPase inhibition, alone and in combination with BET inhibition, as an attractive therapeutic strategy for PRC2-deficient MPNSTs. - Source: PubMed
Publication date: 2026/09/18
Miachin KirillMorgan Marc AlardWang GuangfengMyers Jacquelyn ANavarro John JLempiäinen JoannaLiu XingyuZhou MingzhouYang KuangyingOdhiambo Diana AkinyiHill David W WRoberts Charles W MHirbe Angela CGarcia Benjamin A - Approximately 20% of all cancers contain mutations in genes coding for components of the SWI/SNF chromatin remodeling complex, which exists in three main subtypes: cBAF, PBAF, and GBAF. Mutations in SWI/SNF genes may disrupt chromatin remodeling and deregulate epigenetic processes, leading to aberrant gene expression profiles. However, the gene expression profiles of SWI/SNF genes and subtypes across different tumor types in relation to SWI/SNF mutations remain poorly understood. - Source: PubMed
Publication date: 2026/08/20
Canfjorden VilmaLindén MalinÖsterlund TobiasLarsson ErikStåhlberg Anders - In the histological classification of renal cell carcinoma, clear cell renal cell carcinoma (ccRCC) accounts for the highest proportion and is the most common subtype. Despite advances in management, it continues to be associated with considerable incidence and mortality. Although surgery and systemic therapies are available, their efficacy is constrained by pronounced intratumoral heterogeneity and treatment resistance. Identifying robust biomarkers and clarifying the underlying biological mechanisms are therefore essential to improving diagnosis, risk stratification and therapeutic decision-making. In this work, we identified two ccRCC molecular subtypes displaying divergent chromatin regulator (CR) profiles and different clinical prognoses. Using the genes differentially expressed between these subgroups, we constructed a CR-related score (CRS) that effectively stratified patients according to survival. More analysis concluded that the low expression of CR was more linked with the immune-activated tumors, which encompassed the immune pathway enrichment, as well as the elevation of numerous immune cell subtypes. Moreover, elevated CRS was associated with improved immunotherapy responsiveness. Drug-sensitivity analyses nominated several candidate agents, and SMARCD3 knockdown in 786-O cells inhibited proliferation and migration and reduced sensitivity to masitinib. Collectively, these findings support the prognostic and therapeutic relevance of CR-related states in ccRCC and provide a framework for future experimental validation of chromatin-regulated tumor-immune interactions. - Source: PubMed
Publication date: 2026/08/07
Chen LeiWu QingHong CongTang QilinPan DeshenHe ZhengwenXie Yu - Uterine spiral artery remodelling (SAR) is a fundamental developmental process that facilitates optimal placental perfusion and supports fetal growth. Central to SAR is the phenotypic transformation of vascular smooth muscle cells (VSMCs) from a contractile to a synthetic state, directed by invasive trophoblast cells. To advance these findings, we sought to elucidate the epigenetic mechanisms governing trophoblast-induced reprogramming of VSMC identity, enabling plasticity required for uterine vascular adaptation. - Source: PubMed
Publication date: 2026/07/15
Sarkar PoulomiAin Rupasri - Synthetic gene-regulation logic is established in immortalized cell lines but remains largely aspirational in human induced pluripotent stem cells (hiPSCs) and derivatives. This gap constrains both mechanistic discovery and translational engineering in physiologically relevant models. We developed (ombinatorial nducible CISPR in PSCs), an isogenic, safe-harbor-engineered platform in which tetracycline-responsive single guide RNAs (sgRNAs) carry modular RNA aptamers that recruit RNA-binding proteins and effector domains. This design enables multimodal regulation from a single catalytically inactive Cas9 (dCas9), exemplified by orthogonal CRISPR activation and interference (CRISPRa/i). After optimizing sgRNA-aptamer architectures, we achieved robust CRISPRa and CRISPRi in hiPSCs and hiPSC-derived cardiac organoids. CIRI rapidly channels hiPSC forward programming into skeletal myocytes by activating while repressing , , and . Combinatorial pooled dual-guide single-cell RNA sequencing screens identify as a roadblock and and as synergistic enhancers of myogenic maturation. Together, CIRI establishes a programmable synthetic biology framework in human stem cell models. - Source: PubMed
Publication date: 2026/06/01
Sozza FedericaRomano AlbertoD'Elia NicoleTerenzi MartinaRatto Maria LuisaCliff Emily RNattenberg GabrielleBianchi SaraBecca SilviaKlug HeatherCacchiarelli DavideZalatan Jesse GBalmas ElisaBertero Alessandro