SH3BGRL3 antibody
- Known as:
- SH3BGRL3 (anti-)
- Catalog number:
- orb39997
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- SH3BGRL3 antibody
Related genes to: SH3BGRL3 antibody
- Gene:
- SH3BGRL3 NIH gene
- Name:
- SH3 domain binding glutamate rich protein like 3
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1p36.11
- Locus Type:
- gene with protein product
- Date approved:
- 2001-04-26
- Date modifiied:
- 2016-01-29
Related products to: SH3BGRL3 antibody
Related articles to: SH3BGRL3 antibody
- Identifying new drug targets is essential for improving breast cancer survival. The proteome provides a rich source for potential therapeutic targets. This study aimed to identify protein markers and therapeutic targets for breast cancer by using proteome-wide Mendelian randomization (MR). - Source: PubMed
Publication date: 2025/08/04
Cao ZheXuPeng QiyunTan Shenglan - SH3 Domain Binding Glutamate Rich Protein Like 3 (SH3BGRL3) plays a crucial part in regulating tumor necrosis factor (TNF)-induced effects and was involved in the onset and progression of various cancers. However, its role at pan-cancer level remains unclear. - Source: PubMed
Publication date: 2026/07/21
Yao YuntaoZhao ZihuiLu BingnanZhang HaoyuLyu DonghaoDong KeqingZhu BolinWei MaodongHuang RunzhiLiu YifanPan Xiuwu - Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disorder characterized by unpredictable flares and variable clinical quiescence. Despite validated clinical indices like the British Isles Lupus Assessment Group (BILAG) score, reliable molecular biomarkers for monitoring disease activity remain limited, particularly in underrepresented South Asian populations. Weaimed to identify arobust molecular framework to distinguish SLE flares from remission in an Indian cohort. - Source: PubMed
Publication date: 2026/06/03
Karmakar AbhibrotoMishra SantanuKumar UmaKamath RachanaRavindran VinodSuryakanth Varashree BolarPrabhu SmithaNagaraju Shankar PrasadPrabhu Mukhyaprana MKarmakar Subhradip - OBJECTIVE: This study aims to elucidate the molecular mechanisms by which SH3BGRL3 regulates radiosensitivity and immune evasion in triple-negative breast cancer (TNBC). METHODS: An orthotopic TNBC model was established by injecting 4T1 cells into the mice. In vitro, BT549 cells were co-cultured with CD8+ T cells isolated to mimic the immune microenvironment. Cell proliferation was assessed by CCK-8 and colony formation assays, while migration was evaluated using Transwell. Key protein expression was analyzed by Western blot, immunofluorescence, and immunohistochemistry. RESULTS: Our study revealed that SH3BGRL3 is upregulated in TNBC, where its knockdown suppresses the proliferation and migration of irradiated BT549 cells in vitro and inhibits tumor growth in vivo. Additionally, SH3BGRL3 depletion downregulated ferroptosis-related proteins GPX4 and SLC7A11, elevated Fe²⁺, MDA, and lipid ROS levels, and reduced GSH-effects that were rescued by the ferroptosis inhibitor Fer-1. Our study further demonstrates that SH3BGRL3 knockdown reduces the expression of exhaustion markers (PD-1, TIM-3, LAG-3, TIGIT) on CD8⁺ T cells while increasing the secretion of effector molecules (IFNg, granzyme B, perforin). Notably, we found that Rab27a expression is also upregulated in TNBC, and SH3BGRL3 can bind to Rab27a and stabilize its protein level. Mechanistic studies revealed that knocking down SH3BGRL3 attenuates its interaction with Rab27a and reduces Rab27a expression, thereby promoting ferroptosis and enhancing radiosensitivity, while also inhibiting the Rab27a-mediated exosome release pathway, which in turn enhances CD8⁺ T cell function and suppresses tumor immune escape. CONCLUSION: This study demonstrates that SH3BGRL3 promotes radioresistance and immune evasion in triple-negative breast cancer by regulating Rab27a. - Source: PubMed
Publication date: 2026/04/27
Wang LiLu FeiGao JingyanLi YanliLi SongqinLi ManDong Renyi - Previous genome-wide association studies (GWAS) have identified several risk genes for stroke; however, it remains unclear how they confer risk for the disease. We conducted an integrative analysis to identify candidate genes for stroke and stroke subtypes by integrating blood-derived multi-omics data with genetic data. We systematically integrated the latest stroke GWAS database with human plasma proteomes and performed proteome-wide association studies, Mendelian randomization (MR), Bayesian colocalization analysis and transcriptome-wide association study to prioritize genes that associate the risk of stroke and its subtypes with their expression and protein abundance in plasma. The target genes were verified by performing tissue and cell type specificity, and functional analysis using the Genotype-Tissue Expression database, single-cell RNA sequencing and Gene Ontology databases. A two-step MR analysis was followed to explore the potential mechanisms. We found that the protein abundance of seven genes ( and ) in the plasma was associated with stroke and its subtypes, and six genes ( and ) causally related with stroke and its subtypes. The effect of and on each subtype was mediated by Factor XI inhibitors, atrial fibrillation, type 2 diabetes and systolic blood pressure, respectively ( < 0.05). We also found that and were related to stroke and ischemic stroke at the transcriptome level. Our present proteomic findings may offer potential future therapeutic targets for stroke prevention. - Source: PubMed
Publication date: 2025/12/30
Liu HanchenZhang XiaoxiMa HongyuNguyen Thanh NLing YiMo ShaojunHuang QinghaiLiu JianminZhou YuYang Pengfei