Ask about this productRelated genes to: WASF3 antibody
- Gene:
- WASF3 NIH gene
- Name:
- WASP family member 3
- Previous symbol:
- -
- Synonyms:
- WAVE3, SCAR3, KIAA0900
- Chromosome:
- 13q12.13
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-21
- Date modifiied:
- 2019-02-15
Related products to: WASF3 antibody
Related articles to: WASF3 antibody
- Anal fistula is one of the most common and frequently occurring diseases in the anorectal department. Calvatia lilacina spore (CLS) has been applied for wound treatment with a long history as a traditional Chinese medicine (TCM). However, the mechanism of CLS to treat postoperative wound of anal fistula remains unclear. The present study aims to investigate the efficacy and mechanism of CLS in promoting anal fistula wound healing from the perspective of regulating the interaction between macrophages and fibroblasts. - Source: PubMed
Publication date: 2026/01/07
He TangtangWang KeweiMo RuiwenGuo JuntongJiang BinMu RuoyuMin WenZhu LifengChen Jun - Esophageal squamous cell carcinoma (ESCC) tissues exhibit abnormal N6-methyladenosine (m6A) modification and regulator levels, but the specific effects of this dysregulation on ESCC remain unclear. WASF3 levels were significantly elevated in ESCC tissues, and ESCC patients with high WASF3 expression had significantly worse prognosis. WASF3 suppressed the proliferation of ESCC cells and inhibited colony formation and cell cycle progression. Mechanistically, METTL3 interacted with WASF3 and mediated m6A modification of its mRNA. Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) enhanced WASF3 translation by binding to the m6A site in its 3' untranslated region, and highly expressed WASF3 activated the mitogen-activated protein kinase (MAPK) signaling pathway by interacting with phosphorylated p38 (p-p38), thereby promoting ESCC progression. Moreover, removal of the m6A modification of WASF3 mRNA inhibited WASF3 expression, ESCC cell proliferation, and abolished the ability of WASF3 to bind to p-p38 and activate MAPK signaling. LNP small interfering RNA targeting WASF3, both alone and in combination with paclitaxel, could successfully suppress ESCC tumorigenesis. Our findings demonstrate that WASF3 plays a pivotal role in ESCC and highlight the functional significance of the METTL3/m6A/WASF3/IGF2BP2 axis in regulating ESCC progression, which could facilitate the development of novel prognostic and therapeutic targets for ESCC. - Source: PubMed
Publication date: 2025/10/20
Shang Qi-XinHuang Wen-HuaFeng Yan-RuYang Yu-ShangHu Wei-PengLiu Yi-XinYuan YongJi Ai-FangChen Long-Qi - Wiskott-Aldrich syndrome protein family (WASF) members are key regulators of actin cytoskeleton dynamics at the leading edge of the cell membrane. WASF3 has been demonstrated to directly promote cancer invasion and metastasis in triple-negative breast cancer. WASF3 is incorporated into a heteropentameric protein complex with BRK1, CYFIP1/2, NCKAP1/1L, and ABI1/2/3 termed the WASF Regulatory Complex (WRC) that links upstream signaling pathways to Arp2/3-mediated actin nucleation. Disruption of the complex inhibits actin remodeling and presents a novel approach to targeting cancer invasion and metastasis. Here we report the development of a first-generation all-hydrocarbon stapled BRK1 mimetic peptide, BASH-2, designed to inhibit BRK1 binding within the WRC to disrupt proper WRC assembly and function. BASH-2 was found to permeate cells, bind to WASF3 and ABI2, and inhibit cancer cell migration and invasion in a dose-dependent manner. BASH-2 may present a novel approach to targeting WASF3-promoted invasion and metastasis in triple-negative breast cancer. - Source: PubMed
Publication date: 2025/07/28
Whittaker Matthew KDill Taylor CLimaye Ameya JTsavaris Nicholas JTawadrous Nicholas WKennedy Eileen J - Ischemic stroke (IS), a leading cause of global disability and mortality, is characterized by white matter damage and demyelination. Despite advances, the molecular mechanisms driving post-IS myelin pathology remain poorly understood, limiting therapeutic development. This study investigates key myelin-related genes (MRGs) and their regulatory networks to identify novel therapeutic targets. A transient middle cerebral artery occlusion (MCAO) model was established in C57BL/6 mice, with brain tissues collected at four timepoints (Sham0D, MCAO0D, MCAO7D, MCAO14D). Transcriptomic and proteomic sequencing were performed, followed by soft clustering (Mfuzz), functional enrichment (GO/KEGG), and ROC analysis to identify key MRGs. Competing endogenous RNA (ceRNA) networks were constructed, and drug prediction was conducted using the Comparative Toxicogenomics Database (CTD) and molecular docking. Expression validation was performed via qRT-PCR and Western blot. Integrated multi-omics analysis identified Wasf3 and Slc25a5 as key MRGs, enriched in mitochondrial respiration, calcium metabolism, and cytoskeletal regulation. The AUC values of the one-to-one model scores were all greater than 0.7, suggesting that Wasf3 and Slc25a5 were able to effectively discriminate between samples from different time points. A ceRNA network revealed critical interactions, including the Wasf3-mmu-miR-423-5p-H19 axis, linking apoptosis and myelin dysfunction. Drug prediction highlighted valproic acid (VPA) as a high-affinity binder for both genes (binding energies: - 4.2 and - 4.7 kcal/mol), suggesting its potential as a therapeutic candidate for IS. Experimental validation confirmed significant downregulation of Wasf3 mRNA (p < 0.01) and protein (p = 0.069) post-IS, while Slc25a5 showed no significant changes, potentially due to sample size limitations. This study establishes Wasf3 and Slc25a5 as pivotal regulators of post-IS myelin pathology and proposes VPA as a promising therapeutic candidate to enhance remyelination. The findings underscore the utility of multi-omics approaches in bridging molecular mechanisms to clinical translation, offering new strategies for IS diagnosis and treatment. - Source: PubMed
Publication date: 2025/03/14
Qian QiuyangLyu HaoWang WeiWang QiwenLi DeshengLiu XiaojiaHe YiShen Mei - Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating multisystem disorder of unclear etiology that affects many individuals worldwide. One of its hallmark symptoms is prolonged fatigue following exertion, a feature also observed in long COVID, suggesting an underlying dysfunction in energy production in both conditions. Here, mitochondrial dysfunction and its potential pathogenetic role in these disorders are reviewed. - Source: PubMed
Publication date: 2025/02/17
Syed Abu MohammadKarius Alexander KMa JinWang Ping-YuanHwang Paul M