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
- Acquired resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors remains the principal barrier to durable responses in non-small cell lung cancer (NSCLC), yet how the molecular interaction networks underlying this resistance reorganize over time is poorly understood. We reasoned that a systems-level signature of resistance should be visible in the way protein interaction networks remodel under sustained drug exposure, and therefore applied time-resolved network analysis to isogenic gefitinib-sensitive PC9 and gefitinib-resistant PC9R cells across 24 h of gefitinib treatment, computing network entropy and centrality measures for temporal protein interaction networks and interrogating co-expression-augmented networks for candidate resistance-associated bottleneck proteins. Network entropy rose in both phenotypes, indicating that entropic remodeling is a general response to EGFR pathway perturbation rather than a signature of resistance. In contrast, eigenvector entropy was higher in resistant cells at the earliest post-treatment time point, and resistant cells preserved giant-component connectivity and small-world topology early before fragmenting later. Temporal centrality analysis nominated BIRC3 as a resistant-cell-associated high-centrality node at 24 h, and co-expression analysis identified delta-catenin (CTNND1) as a high-betweenness bottleneck in the PC9R network, topologically bridging EGFR, VAV3, HIF3A, and NOTCH2. These findings nominate early post-treatment eigenvector entropy and a CTNND1-centered, EGFR-enriched subnetwork as candidate resistance-associated features that require validation in independent datasets and functional models. - Source: PubMed
Publication date: 2026/09/21
Tsakona Dimitra CPapanikolaou Nikolaos A - Globally, acute ischemic stroke (AIS) continues to be a major contributor to death and long-term functional impairment. The present work investigates the clinical relevance of miR-369-3p in AIS and how it regulates brain microvascular endothelial cells. Quantitative measurements of serum miR-369-3p were conducted in a cohort comprising 138 individuals with AIS and 120 healthy controls. ROC curve analysis and Cox proportional hazards regression were employed to evaluate diagnostic and prognostic performance of miR-369-3p. Human brain microvascular endothelial cells (hCMEC/D3) were exposed to oxygen-glucose deprivation followed by reoxygenation (OGD/R), allowing assessment of how miR-369-3p influences cell viability, inflammatory responses, and the expression of adhesion molecules. Downstream target genes were identified through bioinformatics analysis and validated using a dual-luciferase assay. A statistically significant reduction in serum miR-369-3p levels was observed among AIS patients relative to controls (P < 0.001), and this miRNA demonstrated favorable diagnostic accuracy. Lower expression of miR-369-3p emerged as an independent predictor of poorer functional outcomes, as assessed by the modified Rankin Scale (mRS) score at 90 days post‑stroke. In cellular studies, upregulation of miR-369-3p mitigated the loss of cell viability induced by OGD/R, reduced the production of pro‑inflammatory cytokines and lowered the levels of ICAM‑1 and VCAM‑1. Furthermore, VAV3 was confirmed as a direct target of miR-369-3p; restoring VAV3 expression counteracted the protective effects conferred by miR-369-3p. Serum miR-369-3p may serve as a non-invasive diagnostic and prognostic biomarker for AIS. Mechanistically, miR-369-3p protects against ischemic endothelial injury by targeting VAV3 and mitigating inflammation and adhesion molecule expression. - Source: PubMed
Publication date: 2026/08/08
Zhang MeijieYin LidaLiu ZhixinMeng YanruLi YueMeng JinhuiYin Xueyong - Autoimmune hypothyroidism (Hashimoto's thyroiditis) is common and has a strong genetic component. Here we performed multi-ancestry genome-wide association meta-analyses encompassing 48,694 Hashimoto's thyroiditis cases, using a precise case definition, and 1,044,134 controls. We identified 155 significant (P < 5 × 10) independent genetic associations, of which 45 variants and 19 loci were not previously associated with hypothyroidism. Six loci were specific for individuals of European ancestry reference populations. Functional enrichment analyses of Hashimoto's thyroiditis-associated genes highlighted immune cells and the spleen, underpinning the importance of T cells in Hashimoto's thyroiditis development. This observation was further supported by 161 significant colocalizations with expression quantitative trait loci in immune cells and 40 in thyroid tissue (for example, TG, VAV3, IRF5), highlighting the interplay between the immune system and the thyroid. Mendelian randomization indicated causal effects of Hashimoto's thyroiditis on cardiovascular traits and expected associations with thyroid hormone levels. - Source: PubMed
Publication date: 2026/07/29
Bujnis Melissa NSterenborg Rosalie B T MLi YongÅsvold Bjørn OlavBrčić LukaBoraska Perica VesnaBabbar AnavDenny Joshua CFritsche Lars GKanai MasahiroKonrade IlzeLeese GrahamMarouli EiriniMetspalu AndresMoksnes Marta RMukherjee BhramarOkada YukinoriPalmer Colin N APapadopoulou AretiPeculis RaitisRovite VitaSauer Peter JSoto-Pedre EnriqueSrinivasan SundararajanSteinbrenner IngaTeder-Laving MarisWang BinWeihs AntoineZeng ChenjieZhou Jin Song XiChengJorde Lynn BMedici MarcoTeumer Alexander - Colorectal cancer (CRC) screening is crucial for early detection, yet the invasiveness of the gold-standard colonoscopy limits compliance. To address the limitation, this study proposes a novel multi-target free DNA methylation model and evaluated its risk stratification performance for CRC in high-risk populations. - Source: PubMed
Publication date: 2026/07/29
Li YingLi ShibaoWang HuiFeng Qian - Extracellular vesicles (EVs) and their miRNA cargo are important regulators of intercellular communication, but their role in connecting respiratory inflammation in asthma with systemic metabolic alterations remains unclear. We hypothesized that HDM-induced allergic inflammation alters selected serum EV-derived miRNAs and that these changes are associated with molecular alterations in lung and adipose tissue. Serum EV-miRNAs from control and HDM-induced allergic rats were isolated by size-exclusion chromatography and analyzed using TaqMan Advanced miRNA Assays. Candidate rno-let-7b-5p targets were integrated with lung and adipose tissue microarray data, validated by qPCR, and assessed in silico using IntaRNA and DMISO. Among the 13 analyzed miRNAs, rno-let-7b-5p showed a nominally significant 1.5-fold increase in serum EVs from allergic rats (unadjusted = 0.03); no multiple-testing correction was applied. and were enriched in lung inflammatory pathways, whereas was downregulated in adipose tissue. qPCR confirmed increased pulmonary expression ( = 0.00802) and reduced adipose expression ( = 0.00034). Computational analyses yielded high-confidence predictions of interactions between rno-let-7b-5p and both genes, which require experimental validation. These preliminary, hypothesis-generating findings suggest that serum EV-associated rno-let-7b-5p may be associated with molecular alterations in the lung and adipose tissue during HDM-induced allergic inflammation. Confirmation in larger independent cohorts is required. - Source: PubMed
Publication date: 2026/07/03
Langwiński WojciechSakrajda KosmaStachowiak ZuzannaNowakowska-Lewicka JoannaKachel MariaCicha EmiliaNarożna BeataSzczepankiewicz DawidKołodziejski PawełPruszyńska-Oszmałek EwaSzczepankiewicz Aleksandra