Ask about this productRelated genes to: SMARCD1 antibody
- Gene:
- SMARCD1 NIH gene
- Name:
- SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily d, member 1
- Previous symbol:
- -
- Synonyms:
- BAF60A, Rsc6p, CRACD1
- Chromosome:
- 12q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1998-05-15
- Date modifiied:
- 2016-10-05
Related products to: SMARCD1 antibody
Related articles to: SMARCD1 antibody
- Three biochemically distinct BRG1 associated factor (BAF) complexes namely canonical (cBAF), poly-bromo (PBAF), and non-canonical (ncBAF) are defined in humans. ARID-domain containing BAF components namely ARID1A, ARID1B (both for cBAF), and ARID2 (for PBAF) define the respective complex assemblies. We previously proposed ARID2's role as a bonafide tumor suppressor in colorectal cancer (CRC), but it's essentiality in maintaining PBAF integrity in CRC remained unexplored. Here, we generated ARID2 knockout HCT116 CRC cells and validated loss of tumor suppression using several cellular and nude mice xenograft assays. Notably, loss of ARID2 led to a marked reduction in PBAF complex assembly, resulting from destabilization of PBAF-specific components BRD7, PHF10, and PBRM1, while core BAF (SMARCD1 and BAF155), ATPase (BRG1), and cBAF (ARID1A) components remained unaffected. Reintroduction of wild-type ARID2 restored PBAF integrity and component levels and reversed the tumorigenic phenotype. Destabilization of PBAF-specific components was also detected upon ARID2 knockdown in HT-29 and SW620 CRC cells. RNA-seq analysis of ARID2 knockout and knockdown CRC cells revealed widespread transcriptional changes affecting disease processes, including CRC and neurodegenerative disorders, as well as cell signaling pathways known to drive CRC, including Wnt/β-catenin, TNFA/NF-κB, and IL2/STAT5; but transcript levels of PBAF-specific components remained unchanged. These results were validated by RT-qPCR. Further, analysis of TCGA RNA-Seq data revealed no significant correlation between transcript levels of ARID2 and other PBAF components. Overall, our study establishes ARID2 as a critical stabilizer of the PBAF complex thus maintaining tumor suppression in CRC. - Source: PubMed
Publication date: 2026/09/19
Sarkar SanjanaSaikia JimleeBashyam Murali Dharan - Long-term memory (LTM) formation requires activated gene expression in response to neuronal activity. Chromatin remodeling is thought to play a role in this transcriptional response, but the mechanisms remain unclear. In Drosophila melanogaster, a transcriptional trace of courtship LTM training can be observed in the mushroom body (MB) during the memory consolidation phase after the end of training. We investigated the role of Bap60, a core subunit of the SWI/SNF chromatin remodeling complex, in the transcriptional trace of memory consolidation. Knockdown of Bap60 in the adult MB impaired LTM. Transcriptome analysis of MB neurons following training revealed disruption of training-induced transcription in Bap60 knockdown MBs. MB-specific CUT&RUN for Brm was used to map SWI/SNF binding sites and identify 142 Bap60-regulated Brm-bound genes. Bap60 was not required for training-induced activation of immediate early genes (IEGs), Hr38 and sr, which encode critical LTM transcription factors. This suggests that Bap60 regulates LTM gene induction downstream of, or in cooperation with IEGs. In support of this, we identified Sr binding sites at 43/142 of Bap60-regulated Brm-bound genes. Among the Bap60 and Sr target genes, we identified prospero, encoding a transcription factor with known roles in MB development. Knockdown of Prospero in the adult MB impaired LTM and Prospero DNA binding sites were identified at 46/142 of Bap60-regulated Brm-bound genes. This suggests that Prospero is an important transcription factor for LTM within the Bap60-regulated gene network. This work implicates Bap60 as a central player in activation of the transcriptional trace of memory consolidation. - Source: PubMed
Publication date: 2026/08/06
Jones Spencer GRaun NicholasBlackwood CalumMiandashti NedaBleeker Shanyn CHenn Abigail LKramer Jamie M - 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 - In vertebrates, SWI/SNF complexes, also known as BRG1/BRM-associated factor (BAF) complexes, come in three major subtypes, canonical BAF (cBAF or BAF), polybromo-associated BAF (PBAF) and non-canonical BAF (ncBAF), that are targeted to different types of chromosomal -regulatory gene expression control elements. Approximately 20% of malignancies exhibit mutations in genes coding for subunits of the SWI/SNF family of ATP-dependent chromatin remodelling complexes. SMARCD is an essential evolutionarily conserved subunit of these complexes in all eukaryotes. Whilst the integral role of SMARCD in targeting and stabilising the SWI/SNF complexes is conserved from yeast to plants to humans, the three human SMARCD paralogs display specific expression patterns underlying their functional divergence. Although, all three SMARCD paralogs exhibit context-dependent roles in cancer, acting as both tumour suppressors and oncogenes, it is SMARCD1 that appears to show the broadest oncogenic footprint across malignancies, driving proliferation, invasion and metastasis in diverse cancer types. Here we review the recent literature pertaining to the molecular and cellular roles of the mammalian SMARCD paralogs and discuss their roles in oncogenesis from those perspectives. - Source: PubMed
Publication date: 2026/06/12
Pere JeromeLogie Colin - Cancer is a complex set of diseases caused by the dysregulation of cell proliferation, differentiation, and apoptosis, ultimately leading to malignant tumor development and metastasis. Recent studies have revealed that dysregulation of N4-acetylcytidine (acC) acetylation is associated with enhanced metastatic potential and tumor progression in various cancer types. However, it remains unclear whether diverse cancer types share common epitranscriptomic regulatory patterns or engage in interconnected networks. - Source: PubMed
Publication date: 2026/05/19
Yin XiangyuTu GangWang XuanLiu YuqiWang YueMa JiongmingYu XiaoXuanMeng JiaSong Bowen