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
- Colorectal cancer (CRC) is a highly prevalent and lethal digestive system malignancy worldwide, which mostly develops through a multi-step progression from normal mucosa to adenoma and finally invasive carcinoma. Lack of specific biomarkers for precancerous lesions limits early screening and intervention efficacy. This study aimed to investigate the differential expression of Dickkopf-related protein 4 (DKK4) in CRC and its correlation with clinicopathological features, and to construct a DKK4-based risk prediction model for CRC. - Source: PubMed
Publication date: 2026/05/27
Wang XiaoxiongShan MinghaiQiao XiaDing LuYang JialiHe FangMian YushenZhang XuYang Shaoqi - Recent transcriptome analysis has demonstrated increased expression of Vascular Endothelial Growth Factor receptor-1 (VEGFR-1/FLT1) and in AD brain. Increased expression of VEGFR1 and its ligand VEGFB were associated with a more rapid rate of cognitive decline, providing evidence of a potential link between increased VEGFR-1 expression in AD pathogenesis. In this study, we explored the potential role of VEGFR-1 expression in neurons on AD pathology. - Source: PubMed
Publication date: 2026/05/29
Mukhopadhyay DebabrataDas PritamAngom Ramcharan SinghDutta ShamitLi ZonghuaCastanedes-Casey MonicaKulkarni TanmayChakravarty TrishaWang EnfengDickson DennisRachamala Hari Krishnareddy - Ischemic stroke (IS) is the most prevalent cerebrovascular disease, with a high proportion of patients developing lifelong disability. Cerebral microcirculatory dysfunction is a key driver of poor IS prognosis. Hypoxia-induced cerebral angiogenesis could improve cerebral perfusion but risks blood-brain barrier (BBB) disruption, worsening outcomes. We previously found that intermittent hypoxia (IH) promotes cerebral angiogenesis and improves IS outcomes, but whether it maintains BBB integrity during angiogenesis and the underlying mechanism remains unclear. This study established mouse hypoxia models, including IH and continuous hypoxia (CH) treatment groups. We found that both IH and CH transiently increased cerebrovascular permeability via angiogenesis activation. However, IH restored permeability to baseline over time, with astrocyte end-foot wrapping, pericyte coverage, and tight junction protein ZO-1 level in neovessels comparable to controls. In contrast, CH failed to recover vascular leakage and BBB integrity within the same period. Mechanistically, IH uniquely activated both hypoxia-inducible factor (HIF)-1α and HIF-2α, while CH only activated HIF-2α. HIF-1α-specific activation in the IH group promoted downstream vascular endothelial growth factor (VEGF)-B transcription, which antagonized VEGFA-mediated endothelial barrier disruption and adhesion molecule upregulation. This study demonstrates that IH maintains neovascular BBB integrity via the HIF-1α/VEGFB pathway, providing a theoretical basis for novel IS interventions and targeted drug development. - Source: PubMed
Publication date: 2026/06/13
Cao MingxuanXu ZiruiGu YakunZhang QihanGuo MengyuanTian ZhengmingJin FeiyangShao QianqianGuo XiuhaiLiu JiaJi Xunming - Endometriosis is a prevalent gynecologic disorder that significantly impacts women's health. However, its underlying pathogenesis remains unknown. This study aimed to ascertain causal associations between plasma protein levels and endometriosis using a Mendelian randomization (MR) design. Plasma protein genome-wide association studies (GWAS) data originating from the UK Biobank Pharma Proteomics Project (UKB-PPP) were utilized as exposure variables. Endometriosis GWAS data from the FinnGen study and UKB study served as outcome variables at the discovery and replication stages, respectively. Summary-data-based MR (SMR) and instrument-dependent heterogeneity (HEIDI) tests were conducted to further validate the relationships between proteins and the risk of endometriosis. Genetic variations between the identified plasma proteins and endometriosis were investigated by colocalization analyses. The proteome‑wide MR and SMR results revealed that genetically predicted plasma levels of proteins (RSPO3, WASHC3, FSHB, and VEGFB) were positively associated with the risk of endometriosis. Among them, only FSHB and RSPO3 passed the HEIDI tests, and colocalization analyses further supported their causal relationship with endometriosis. Based on large-scale population GWAS data, our research demonstrated causal correlations of FSHB and RSPO3 with the risk of endometriosis. These findings suggest that plasma proteins are involved in the development of endometriosis and may serve as potential biomarkers and therapeutic targets for this complicated disease in the future. - Source: PubMed
Yao XiangXu WenjuanWang ZhijuanGao QunWang JianyeZhou Ping - Sleep deprivation induces systemic physiological stress accompanied by transcriptomic remodelling and immune dysregulation, yet objective molecular indicators for its assessment remain insufficient. This study integrated blood transcriptomic analysis with an interpretable machine learning framework to identify and validate candidate molecular signatures associated with sleep deprivation and their potential relevance to insomnia. Publicly available Gene Expression Omnibus datasets were used to construct an acute sleep deprivation training cohort, an independent sleep deprivation validation cohort, and a chronic insomnia validation cohort. Differentially expressed genes were first identified, followed by feature selection using six machine learning algorithms and Shapley additive explanations to improve model interpretability. Immune cell composition was inferred using CIBERSORT, and associations between candidate genes and immune cell subsets were further evaluated. Twenty-five differentially expressed genes were identified in the training cohort, from which eight high-priority candidate genes were selected by the interpretable machine learning framework. Among them, S100A3 showed consistent discriminatory performance across the training cohort, the independent sleep deprivation cohort, and the insomnia cohort, whereas VEGFB exhibited notable diagnostic potential, particularly in insomnia. Immune infiltration analysis indicated that sleep deprivation was associated with altered peripheral immune composition, including reduced resting natural killer cells and activated dendritic cells, together with changes in regulatory and naïve immune cell populations. Expression levels of S100A3 and VEGFB were significantly correlated with specific immune cell subsets, suggesting a link between these molecular signatures and stress-related immunomodulation. These findings identify S100A3 as a robust candidate biomarker shared by acute sleep deprivation and chronic insomnia, while VEGFB may reflect chronic metabolic or inflammatory adaptation. The proposed interpretable transcriptomic-machine learning framework provides a non-invasive strategy for discovering molecular indicators of sleep-related physiological stress and may support future risk stratification in sleep medicine. - Source: PubMed
Wang KunZong QiangWang ChengchengWang PengShuai ZhenhaoWu MinPeng YumingZhou JunyingShuai JianweiYe FangfuWu AiminZheng Yanyan