Ask about this productRelated genes to: VEGFB antibody
- Gene:
- VEGFB NIH gene
- Name:
- vascular endothelial growth factor B
- Previous symbol:
- VRF
- Synonyms:
- VEGFL
- Chromosome:
- 11q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-10-26
- Date modifiied:
- 2015-07-22
Related products to: VEGFB antibody
Related articles to: VEGFB antibody
- Vascular endothelial growth factor (VEGF) signalling mediates pleiotropic effects within the brain, encompassing angiogenesis, neuronal survival, and immune signalling. There is growing interest in the role of VEGF signalling in the pathophysiology of Alzheimer's disease (AD). The generation of single-cell brain atlases and recent large multi-omic studies, including analysis of CSF and bloods alongside post-mortem brain tissue, have provided novel insights into the role of VEGF signalling in AD. Disruption of the VEGF-A/VEGFR2 signalling pathway, due in part to elevated soluble VEGFR1 expression may contribute to pathogenic angiogenesis, BBB leakiness, and neuronal loss in AD. Induction of VEGF-B/VEGFR1 signalling in microglia suggests that dysregulated VEGF-mediated immune cell signalling is a further influence on AD pathogenesis. A reduction in expression of the 'protective' VEGFR3 and co-receptors neuropilin 1 and 2 has also been recently linked to cognitive decline in AD. In large clinical studies, lower VEGF-A levels in CSF and serum, raised soluble VEGFR1in CSF and elevated PlGF in CSF and serum, are predictive of more rapid cognitive decline and accelerated Alzheimer's disease neuropathological change (ADNC). This review discusses findings from recent multi-omic studies of large clinical and neuropathological studies that prompt reconsideration of the nature of VEGF signalling in AD and shed light on some of the complexities and previous conflicts within the field. - Source: PubMed
Publication date: 2026/04/12
Emery Cherelle E GLove SethMiners J Scott - PRCC-TFE3 rearranged renal cell carcinoma (PRCC-TFE3 rRCC) is a highly malignant renal malignancy with limited therapeutic options, underscoring the urgent need for novel treatment strategies. - Source: PubMed
Publication date: 2026/04/07
Liu XuwentaiChen YiLiu WujiaPan JunLiu JiaxinDong XiangMa WenliangFeng FanLiu NingXu JingyuanGan WeidongLi Dongmei - Sirtuin 3 (SIRT3), a mitochondrial NAD-dependent deacetylase, plays a central role in regulating mitochondrial metabolism, oxidative stress, and cell survival. Although SIRT3 has been implicated in angiogenesis, apoptosis, and inflammation, its global proteomic impact on the brain remains unclear. This study aimed to systematically characterize alterations in angiogenesis-, apoptosis-, chemokine-, and cytokine-related proteins in the brains of SIRT3 knockout (SIRT3 KO aka SIRT3/) mice compared with wild-type (WT) controls. - Source: PubMed
Publication date: 2026/02/28
He QingpingKhan SamiaWang LinlinIbeanu Gordon CLi P Andy - Dual inhibition of PD-1/PD-L1 and VEGF/VEGFR pathways is a promising strategy to overcome tumor immune evasion and inhibit angiogenesis. IMM2510 is a novel PD-L1 × VEGF bispecific antibody, constructed by fusing VEGFR1 domain 2 (VEGFR1D2) to each anti-PD-L1 heavy chain. In addition, IMM2510 incorporates an Fc region engineered for enhanced antibody-dependent cellular cytotoxicity (ADCC), enabling elimination of PD-L1-expressing tumor and stromal cells. - Source: PubMed
Publication date: 2026/01/15
Chen DianzeWu ZhuliZhao XiwenBhatt Rupal SYang YananZhu WenqiTang HuangWang KailiGuo ChunliLiu DandanYang ChunmeiGuo HuiqinBai XingZhang RuliangLi SongTian Wenzhi - Diabetes affects over half a billion people worldwide, with cardiovascular disease being its leading cause of death, either occurring secondary to atherosclerosis or due to an intrinsic defect in heart muscle (diabetic cardiomyopathy, DbCM). One instigator for DbCM is impaired cardiac metabolism characterized by excessive fatty acid (FA) delivery and utilization by the heart, causing oxidative stress and toxic lipid accumulation. Inhibition of vascular endothelial growth factor B (VEGFB) has been shown to counter these factors associated with abnormal cardiac metabolism by inducing metabolic flexibility and preventing cardiac lipid accumulation in Type 2 diabetes. However, its impact on lipoprotein lipase (LPL) and the sources of FA for cardiac use in Type 1 diabetes is unknown. Global knockout (Vegfb) in rats caused limited phenotype and cardiac transcriptome changes under normal conditions but notably reduced cardiac LPL activity, probably by impeding LPL translocation from cardiomyocyte to the coronary vasculature. Under streptozotocin (STZ)-induced diabetes, Vegfb rats exhibited increased cardiac LPL activity, protecting animals from dyslipidemia, decreased plasma saturated FA, and provided a safer cardiac FA source, LPL-derived FA. Knockout of also protected animals from DbCM by inhibiting excess FA oxidation, preserving angiogenesis and alleviating cell death in the heart. Inhibiting VEGFB may offer a promising therapeutic approach to address the current lack of mechanism-based treatments for DbCM. - Source: PubMed
Publication date: 2026/02/18
Wang HualinShang RuiLee Chae SyngHussein BahiraRodrigues Brian