Ask about this productRelated genes to: VEGFB Blocking Peptide
- 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 Blocking Peptide
Related articles to: VEGFB Blocking Peptide
- Prostate cancer is among the most prevalent malignancies in men and a leading cause of cancer mortality worldwide. While localized prostate cancer is often curable, progression to metastatic and castration-resistant disease either in lymph nodes or bone/bone marrow remains the major cause of death. Understanding the genomic events that drive metastasis-particularly in treatment-naïve patients-is critical to improving early detection and individualized therapy. Bulk tumor sequencing has revealed key mutational signatures but cannot resolve the cellular heterogeneity and clonal dynamics underlying metastatic spread. Single-cell genomic approaches now enable high-resolution dissection of tumor evolution, uncovering the diversity of cancer clones across disease sites. - Source: PubMed
Publication date: 2026/05/08
Jovel JuanPolzer BernhardPatterson JordanYong HouVasquez CatalinaO'keefe SandraPink DesmondLi GuiboFairey AdrianAdam BenjaminTeitelbaum JeremySalimi AmirKirsh StefanAlberter BarbaraLowes LoriCarpenter EricKolinsky MichaelZhu ZhongyiZhou QingVenner PeterVenner ChristopherWilliams DavidAllan AlisonBoutros Paul CKlein Christoph AWong GaneLewis John D - Gastric cancer (GC) remains a leading cause of cancer-associated deaths globally, particularly in East Asia. Although anti-angiogenic therapies have yielded therapeutic benefit in GC, their efficacy is limited, as current vascular endothelial growth factor-A (VEGF-A) and VEGF receptor-2 (VEGFR-2) targeted therapies eventually fail due to compensatory pathways involving VEGF-B and placental growth factor (PlGF). PB101, a VEGFR-1 decoy receptor, inhibits VEGF-A, VEGF-B, and PlGF, potentially offering broader anti-angiogenic effects. This study evaluated the efficacy of PB101 alone and in combination with cytotoxic chemotherapeutic agents in GC models. - Source: PubMed
Park MinsungLee Cheng HyunKim Kui-JinHwang Sung-HyunSung Ji HeaNam MilangKang MinsuPark WoochanKim Ji-WonKim Jin WonKim Se HyunSeo JeongminJung Eun HeeSuh Koung JinKim Yu JungKim Jee HyunLim Hye SeongYang Hyun GulCho Eun ByulLee Keun-Wook - 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