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
- 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 - Sarcopenia refers to the involuntary loss of skeletal muscle mass and function with aging and is associated with multiple adverse health outcomes. Disruption of normal circadian rhythms due to shift work or nocturnal lifestyle is associated with the risk of several diseases such as metabolic syndrome and cancer. However, its role in sarcopenia remains unclear. The synergy of single-cell RNA sequencing and Mendelian randomization (MR) analysis provides an opportunity to reveal the important involvement of circadian rhythms in the pathogenesis of sarcopenia. Data quality control and normalisation were performed in the single-cell dataset, GSE167186. Then, different cell types were obtained by cell annotation through marker genes. Differentially expressed genes (DEGs) were further analyzed in different cell types. The intersection of DEGs and circadian-related genes in fast skeletal muscle cell were taken. Afterwards, the genes that had causal relationship with sarcopenia were selected as biomarkers by MR analysis. Variations in signaling pathways between different cell types were further analyzed. In GSE167186, 20 different cell populations identified by UMAP cluster analysis were further annotated to 8 cell types using maker genes. Afterwards, 44 DEGs were screened between fast skeletal muscle cell and circadian-related genes. Further MR Analysis yielded three genes with significant causal association with sarcopenia, which could be used as biomarkers in this study. SMARCD3 was found to have a protective effect against sarcopenia (OR = 0.9183, 95% CI = 0.8577-0.9832, p = 0.0144); in contrast, CPED1 (OR = 1.0292, 95% CI = 1.0089-1.0500, p = 0.0047) and FNBP4 (OR = 1.1096, 95% CI = 1.0316-1.1934, p = 0.0051) were associated with an increased risk of sarcopenia. The analysis of intercellular signaling revealed that the loss of the protective factor SMARCD3 in fast skeletal muscle cell triggers a specific upregulation of EGF signaling directed at FAPs. This study highlights the contribution of circadian rhythms in the pathogenesis of sarcopenia and further defines circadian rhythm-related biomarkers in sarcopenia, as demonstrated by MR analysis and scRNA-seq analysis. This suggests circadian rhythms as a focal point for pathogenesis research and potential therapeutic targeting in sarcopenia. - Source: PubMed
Publication date: 2026/05/11
Huang YuliTang LifengLi DaoyuanChen LongWu WenjuanZeng DingchengZhong YanbiaoWang Maoyuan - We previously demonstrated that fibroblasts can be reprogrammed through a proliferative progenitor stage to drive both cardiomyogenesis and neovascularization. However, it remains to be determined whether cardiac fibroblasts (CFs), the primary mediators of post-injury remodeling, retain the plasticity to be concurrently redirected into cardiovascular lineages within the environment. - Source: PubMed
Publication date: 2026/04/22
Dutta SuchandrimaChen SophieAhmad WaqasHuang WeiWang YigangLiang Jialiang