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
- Gα is a critical mediator of cell and tissue responses to G-coupled receptor stimulation. Canonically, active Gα regulates PLCβ and RhoGEFs. To identify novel Gα signaling partners, we performed a proximity labeling proteomic screen in HEK293A cells using TurboID-tagged Gα. Top Gα enriched proteins included known Gα interactors (PLCβs, RhoGEFs, and GRK2), supporting the validity of this approach. Also highly enriched were several nuclear proteins including SMARCD3, a component of the SWI/SNF chromatin remodeling complex, and BCAS2, a component of the spliceosome. Luciferase complementation experiments show that Gα selectively interacts with BCAS2 and SMARCD3 in an activation-dependent manner, and pulldown experiments with purified components demonstrate direct interaction of Gα and SMARCD3. We also show that a small but significant portion of Gα is present in the nucleus, and this is increased following GPCR activation or introduction of an activating mutation. Proximity ligation assays indicate that Gα engages SMARCD3 in the nucleus. These data suggest that Gα engages downstream targets in the nucleus and could therefore directly regulate nuclear processes. - Source: PubMed
Publication date: 2026/02/25
Loomis JosephChandan NaincyBurroughs MichaelAbraham SajiZhang RongxiCao YiyiBrody Matthew JTall Gregory GSmrcka Alan V - Mammalian switch/sucrose nonfermenting (mSWI/SNF) chromatin remodeling complexes modulate DNA accessibility and gene expression; however, their genomic targeting mechanisms remain incompletely understood. Here, we identify SWIFT [SWI/SNF immunoglobulin fold (Ig-fold) for transcription factor interactions], a conserved transcription factor (TF) binding domain on the SMARCD subunits. SWIFT is necessary and sufficient for direct engagement with the transactivation domain of the PU.1 TF. A single amino acid mutation disrupts PU.1-mSWI/SNF binding, impairs complex targeting, and attenuates oncogenic transcription and proliferation in PU.1-dependent human cancer cells. Dominant expression of the SWIFT domain in isolation sequesters TFs from mSWI/SNF and poisons TF-"addicted" cancer cells. Finally, TFs across diverse families interact with SMARCD paralog-specific SWIFT domains. These results define a major mechanism of cell type- and disease-specific mSWI/SNF chromatin targeting and inform approaches toward therapeutic modulation. - Source: PubMed
Publication date: 2026/04/02
Jain Siddhant UWilliamson Kaylyn EYing Alexander WTurner Aasha MJiang Ruidong JerryRaval ShaunakSo KevinAllison Maxwell JSankar AkshaySáme Guerra Daniel DLin YutongJiang ZheMashtalir NazarRohrs Henry WLichti Cheryl FMuir Tom WPapanastasiou MalvinaPaulo Joao AGygi Steven PGross Michael LKadoch Cigall - Estrogen receptor-positive breast cancer (ER+BC) accounts for ∼70% of all breast tumors, and 20%-40% of patients develop metastases. Everolimus is an mammalian target of rapamycin (mTOR) inhibitor used in combination with exemestane for metastatic ER+BC. However, resistance remains common and leads to poor survival outcomes. To uncover resistance mechanisms, we analyze transcriptomic profiles from everolimus-sensitive and -resistant ER+BC cell lines. Our study uncovers persistent activation of a growth-factor signaling meta-phenotype in resistant cells involving IGF1R, ESR1, and mitogen-activated protein kinase (MAPK) pathways. We identify SMARCD3 regulons linked to this meta-phenotype. Additionally, we find SMARCD3 regulon activity elevated in everolimus-refractory patient tumors. Importantly, we show that SMARCD3 regulon activation was correlated with sensitivity to several known MEK1/2 inhibitors, including trametinib. Combining trametinib with everolimus treatment significantly reduces resistant cell growth. Our results demonstrate that everolimus-resistant ER+BC cells evade therapy via alternate growth-factor signaling linked to activation of SMARCD3 regulons, which can be therapeutically targeted using MEK1/2 inhibitors. - Source: PubMed
Medina Eric FFarmaki ElenaGriffiths Jason IBild Andrea HNath Aritro - The rumen epithelium, liver, and muscle tissues are key metabolic organs in ruminants, each performing distinct yet interconnected roles in energy metabolism and growth. However, how these tissues coordinate their gene expression to meet metabolic demands in Hu sheep remains poorly understood. - Source: PubMed
Publication date: 2025/11/14
Jia XiaoweiLi JiaxiaoZhang YuanxinTian BoyaMao ShengyongLiu JunhuaQian Wenxi - : Epithelial-mesenchymal transition (EMT) is a fundamental process that drives invasion and metastasis in patients with diffuse-type gastric cancer (DGC). The role of SMARCD3, a subunit of the SWI/SNF chromatin remodeling complex, in this process is largely unknown. The aim of this study is to elucidate the molecular mechanism through which SMARCD3 integrates with the PI3K-AKT and WNT/β-catenin signaling pathways to promote EMT and gastric cancer progression. : Stable SMARCD3-overexpressing MKN45 and MKN74 cell lines were established. RNA sequencing (RNA-seq) was performed to investigate signaling alterations. Western blot analysis confirmed the expression of EMT markers (Snail and Slug) and the phosphorylation of AKT (Ser473) and GSK3β (Ser9). PI3K dependency was tested using the inhibitor LY294002. Cooperative effects were examined by activating the WNT pathway with WNT3A. : SMARCD3 overexpression upregulated PI3K-AKT and WNT signaling, which correlated with increased Snail/Slug expression and increased AKT/GSK3β phosphorylation. GSK3β inactivation (pSer9) stabilizes Snail, driving EMT. LY294002 treatment suppressed Snail/Slug expression, attenuated AKT activation, and reversed the mesenchymal phenotype. Furthermore, WNT3A treatment synergistically increased nuclear Snail accumulation. : SMARCD3 acts as a critical epigenetic regulator that promotes EMT in patients with gastric cancer through the integration of the PI3K-AKT and WNT/β-catenin pathways. Targeting this SMARCD3-mediated mechanism offers a promising therapeutic strategy to inhibit metastasis and improve outcomes for patients with gastric cancer. - Source: PubMed
Publication date: 2025/10/31
Park Ji-HoPark Sun YiJung Eun-JungJu Young-TaeJeong Chi-YoungKim Ju-YeonPark TaejinPark MiyeongLee Young-JoonJeong Sang-Ho