VAV3 antibody
- Known as:
- VAV3 (anti-)
- Catalog number:
- orb101249
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- VAV3 antibody
Related genes to: VAV3 antibody
- Gene:
- VAV3 NIH gene
- Name:
- vav guanine nucleotide exchange factor 3
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-07-07
- Date modifiied:
- 2015-11-27
Related products to: VAV3 antibody
Related articles to: VAV3 antibody
- Dysregulation of microRNAs (miRNAs) has been associated with podocyte injury in diabetic nephropathy (DN). This study aimed to investigate the role and underlying mechanism of miR-208a-3p in the development of DN. An in vitro DN model was established by treating podocytes with high glucose (HG). Gene expression was analyzed using reverse transcription quantitative polymerase chain reaction, and protein levels were determined by Western blotting. Immunofluorescence staining was performed to assess microtubule-associated protein 1A/1B-light chain 3 (LC3) intensity as an autophagy marker. Podocyte viability and apoptosis were evaluated via Cell Counting Kit-8 assay and flow cytometry, respectively. Intracellular reactive oxygen species (ROS) levels were measured using 2',7'-dichlorofluorescin diacetate staining. miR-208a-3p was significantly upregulated in HG-stimulated podocytes. HG exposure promoted apoptosis and oxidative stress, while suppressing autophagy and cell viability, effects that were reversed by miR-208a-3p inhibition. Mechanistically, miR-208a-3p directly targeted vav guanine nucleotide exchange factor 3 (VAV3). HG suppressed AKT/mTOR signaling, whereas miR-208a-3p silencing activated it. Conversely, VAV3 knockdown inactivated AKT/mTOR signaling. VAV3 downregulation or treatment with LY294002, an AKT/mTOR inhibitor, abolished the protective effects of miR-208a-3p silencing against HG-induced podocyte injury. These findings indicate that miR-208a-3p silencing attenuates HG-induced podocyte injury by promoting autophagy via targeting the VAV3/AKT/mTOR pathway. - Source: PubMed
Wang MengjieChen ZhenMa RuiRen YongdongChen HairuiLi LiLv XiaoyuZhang XuyanWang ZhongjingLi Jing - Atherosclerosis is a major cause of ischemic stroke and is characterized by complex immune-metabolic dysregulation. VAV3, a Rho guanine nucleotide exchange factor, regulates multiple cellular processes, but its role in vascular pathology remains unclear. This study aimed to explore the function and mechanism of VAV3 in atherosclerosis. - Source: PubMed
Publication date: 2026/06/04
Wang GuorongPu ChenLi QingLiu QiangWan XiaobinDeng JunDai MinXie BinHuang LianghuiZhao YanPing - Accumulating evidence indicates that indirubin exerts inhibitory effects on prostate cancer (PCa) progression. However, the role and underlying mechanisms of indirubin in sensitizing PCa to docetaxel remain unclear. CCK-8 assays were initially used to determine the effect of indirubin on enhancing docetaxel sensitivity in PCa cells. Following this, the expression levels of circ-Vav3 were quantified using quantitative real-time PCR (RT-qPCR) to evaluate its potential role in docetaxel resistance. Functional experiments, including flow cytometry-based apoptosis analysis and Transwell migration/invasion assays, were conducted to assess the impact of circ-Vav3 modulation and indirubin treatment on cell viability and behavior in response to docetaxel. Rescue experiments were subsequently performed to further confirm the regulatory effect of indirubin on circ-Vav3. Additionally, xenograft tumor models in nude mice were utilized to evaluate the therapeutic efficacy of indirubin in vivo. Mechanistic interactions between circ-Vav3, miR-204-5p, and MAPK1 were further investigated using RNA pulldown assays, luciferase reporter assays, and Western blot analyses. Indirubin enhanced the sensitivity of PCa cells to docetaxel by downregulating the expression of circ-Vav3, which was found to be significantly upregulated in docetaxel-resistant PCa cells. Silencing circ-Vav3 effectively reversed this resistance, as evidenced by increased apoptosis, reduced cell migration and invasion, and decreased autophagic activity. Notably, indirubin treatment suppressed circ-Vav3 expression and thereby restored docetaxel sensitivity both in vitro and in xenograft tumor models. Mechanistically, circ-Vav3 acted as a competing endogenous RNA (ceRNA) by sponging miR-204-5p, which led to the upregulation of the autophagy-related kinase MAPK1. Inhibition of MAPK1 effectively suppressed autophagy and re-sensitized docetaxel-resistant PCa cells, further confirming the critical regulatory role of the circ-Vav3/miR-204-5p/MAPK1 signaling axis in mediating chemoresistance. Our findings demonstrate that circ-Vav3 promotes docetaxel resistance in PCa by sponging miR-204-5p and subsequently activating MAPK1-mediated autophagy. Indirubin effectively restores chemosensitivity by targeting this regulatory pathway, offering a promising therapeutic strategy for overcoming chemoresistance in castration-resistant prostate cancer (CRPC). - Source: PubMed
Zheng MinghaoCai GanMa LongWu XianWang QianJin ZhenhuaZhu ChenNiu ShuaiyuPeng YanpeiXu YanTang JingyuanWei Yunfei - Myocardial infarction (MI) continues to be a leading cause of global mortality. Resibufogenin (RBG), a principal bioactive constituent derived from Venenum Bufonis, is well recognized for its potent cardiotonic properties. Nevertheless, the therapeutic potential of RBG in the context of MI remains to be fully elucidated. This study revealed that RBG exerted significant cardioprotective effects in a murine model of MI by preserving cardiac function, attenuating myocardial injury, and increasing vascular density. Proteomic analysis revealed that angiogenesis was the predominant biological process associated with RBG-responsive proteins. Integrated proteomic analysis and mechanistic validation demonstrated that RBG activated the ITGA5-VEGF signaling axis, a pathway essential for its therapeutic efficacy, in a macrophage-dependent manner. Notably, both pharmacological inhibition of ITGA5 and depletion of macrophages completely abrogated RBG-mediated cardioprotection in the MI model. Furthermore, RBG significantly increased endothelial cell proliferation, migration, and tube formation in a macrophage-endothelial cell coculture system. More importantly, RBG upregulated ITGA5 expression in macrophages through activation of the VAV3/CDC42 signaling pathway. Collectively, these findings demonstrate that RBG is a promising therapeutic agent for myocardial infarction and acts via the macrophage-specific VAV3/CDC42-mediated ITGA5/VEGF signaling pathway to promote reparative angiogenesis. This study elucidates the cardioprotective effects and underlying mechanisms of RBG and establishes a scientific basis for the discovery of novel therapeutic agents from natural products. - Source: PubMed
Publication date: 2026/04/29
Wang RanLin Guo-QiangWang Fei-YunChen YaoPeng Shou-JiaoZhang Jian-Ge - Acute respiratory distress syndrome (ARDS) and acute lung injury (ALI) are characterised by increased pulmonary capillary permeability, but lack effective pharmacotherapies. Emerging evidence implicates gut-lung axis dysregulation in ARDS pathogenesis through microbiome-host interactions, but the specific role of the microbiota-derived metabolite, trimethylamine-N-oxide (TMAO), remains unclear. - Source: PubMed
Publication date: 2026/04/23
Wang XilongZeng WeiyongBai QianwenZhong KaiLuo QiaoDeng JiaCen ChunxianWang KaiLi RuiLi JiehongZhang JingyiYe TiaofeiFang NianxinChen XinWang Tao