Ask about this productRelated genes to: VEGFA antibody
- Gene:
- VEGFA NIH gene
- Name:
- vascular endothelial growth factor A
- Previous symbol:
- VEGF
- Synonyms:
- VEGF-A, VPF
- Chromosome:
- 6p21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-01-10
- Date modifiied:
- 2016-10-05
Related products to: VEGFA antibody
Related articles to: VEGFA antibody
- To explore the molecular mechanisms underlying cystoid macular edema (CME) through protein-protein interaction (PPI) network analysis, identifying key regulatory proteins, functional modules, and enriched biological pathways relevant to its pathogenesis. - Source: PubMed
Shariati Mehrdad Motamed - To clarify the molecular mechanisms through which lobetyolin (LT) modifies the gut microbiota-bile acid axis to multitarget the regulation of hyperandrogenism, insulin resistance, chronic low-grade inflammation, and endometrial dysfunction, consequently breaking the vicious cycle and improving the pathological phenotype of polycystic ovary syndrome (PCOS), thereby establishing a theoretical basis and experimental validation for the advancement of LT as a systemic therapeutic agent for PCOS. - Source: PubMed
Publication date: 2026/05/01
Li LijuanLin PingpingLiu SiyuanZhang YuningWang SiqiLiang JingtaoWang RuyuDuan GuofengChen Aixiang - A high rate of metastasis remains a challenge for the treatment of adenoid cystic carcinoma (ACC), yet the underlying mechanism of lung metastasis remains elusive. By integrating single-cell RNA sequencing and bulk transcriptomics with multiplex immunohistochemistry, we identified a metastatic niche consisting of IL1B tumor-associated macrophages (TAMs), CD24 luminal-like tumor cells, ACKR1 endothelial cells (ECs) and HSPA1ACD8 T cells. Importantly, we revealed that IL1B TAMs play diverse roles in the processes of tumor cell intravasation and colonization, two fundamental steps supporting metastatic outgrowth. In primary lesions, IL1B TAMs release elevated levels of VEGFA and MMPs, thereby coupling sprouting angiogenesis with extracellular matrix remodeling to facilitate cancer cell intravasation. In metastatic lesions, IL1B TAMs bind to IL-1R1 on ACKR1 ECs to upregulate the expression of the adhesion molecule SELP, which can attract CD24 luminal-like tumor cells for lung colonization. IL1B TAMs also increase the stress response state of HSPA1ACD8 T-cell recruitment and induce T-cell exhaustion, thereby facilitating the survival of disseminated tumor cells. Mechanistically, MIF derived from CD24 tumor cells increases the transcription of IL1B in TAMs. We also reported that the infiltration of IL1B TAMs increased steadily with increasing lung metastatic progression in mice bearing metastatic ACC cells. Elevated plasma IL-1β and VEGFA levels are associated with increased metastatic burden and poor overall survival in patients with ACC. Our findings reveal the critical role of IL1B TAMs in reshaping the metastatic tumor immune microenvironment and reveal a potential therapeutic vulnerability for metastatic ACC. - Source: PubMed
Publication date: 2026/05/16
Wang YuZheng JianweiZhang KungeMo WeipengYang XiaotianCui PengyuLiu ChaoZheng LeiXia ShunjinSun MengyuWang BoMei MeiZhou XuanRen Yu - Glioblastoma (GBM) almost inevitably recurs within 6-12 months after standard temozolomide-radiotherapy (TMZ-RT) treatment, frequently transitioning to aggressive mesenchymal (MES) states through non-genomic transcriptional reprogramming. Mutations in p53/TP53 are frequent in recurrent GBM, disabling its tumor suppressor transcriptional activity. In contrast, the related p53 family member, TP63, is rarely mutated in cancers and has been linked with MES maintenance, stemness, and therapy resistance. However, TP63 exhibits context-dependent tumor-suppressive or oncogenic roles, and its relevance to GBM recurrence remains unclear. - Source: PubMed
Publication date: 2026/05/12
Martell EmmaKuzmychova HelgiGrewal AkaljotChawla UjalaJain CharulVenugopal ChitraAnderson Christopher MSingh Sheila KSharif Tanveer - Gastric cancer has remained as a top ranked human malignancy showing both high morbidity and mortality, especially in Asian countries. Recent advances have revealed actionable targets for clinical gastric cancer therapy, including epidermal growth factor receptor 2 (HER2) and vascular endothelial growth factor receptor (VEGFR), thus calling for further investigation of potential therapeutic targets. Platelet-activating factor acetylhydrolase IB subunit alpha1 (PAFAH1B3) functions to remove the acetyl group from platelet-activating factor and is implicated in multiple diseases including cancer. However, the exact roles and underlying mechanisms of PAFAH1B3 in gastric cancer are incompletely investigated. By combining bioinformatic and gastric cancer tissue analyses, we confirmed that PAFAH1B3 was upregulated in gastric cancer and reversely correlated with patient prognosis showing significant association with tumor stages and metastasis. PAFAH1B3 knockdown rendered suppressed proliferation and migration, but enhanced apoptosis of gastric cancer cells. Transcriptomic profiling of control and PAFAH1B3 knockdown cells revealed VEGFA as a downstream effector, the overexpression of which effectively rescued defects imposed by PAFAH1B3 knockdown. Further investigation showed that PAFAH1B3 coordinated with the transcription factor E2F8 to promote VEGFA transcription. Importantly, in xenograft animal models, PAFAH1B3 overexpression significantly enhanced tumorigenesis, while VEGFA knockdown effectively suppressed gastric cancer xenograft growth. Therefore, our findings suggest that the PAFAH1B3/E2F8/VEGFA pathway plays an important role in gastric cancer progression, which can be targeted to design novel therapeutic strategies against gastric cancer. - Source: PubMed
Publication date: 2026/05/14
Liu ZhenhuaXiu YufangZhang ShanniJiang KeqiuZhang XiaoWang HaoDu JianyuZhang YingqiuKong Meng