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vitreous levels increased in neovascular retinal diseases
High plasma VEGF-B levels are associated with type 2 diabetes mellitus.
Data from clinical studies point out the changes in circulating or tissue expression levels of VEGF-B in obese compared with lean patients.
Cardiac transgenic vascular endothelial growth factor-B overexpression failed to protect heart transplants from ischemia-reperfusion injury.
renal VEGF-B expression correlates with the severity of Diabetic Kidney Disease.
Data show that metformin treatment reduces serum vascular endothelial growth factor B (VEGF-B) levels and ameliorates insulin resistance.
VEGFA and VEGFB associated sub-network, kinase insert domain receptor (KDR), fibronectin 1 (FN1), transforming growth factor beta induced (TGFBI) and proliferating cell nuclear antigen (PCNA) found to interact with at least two of the three hub genes.
Frameshift mutations of VEGFB gene is associated with stomach and colorectal cancers.
plasma VEGF levels before treatment were lower in patients with schizophrenia and that their VEGF levels increased after treatment.
fluid shear stress induces the synthesis of Insulin growth factor-2 and vascular endothelial growth factor (VEGF) B and D, which in turn transactivate MMP-12.
MMP9 may activate VEGF-B via PI3K/Akt signaling pathway.
Roles of vascular endothelial growth factor in amyotrophic lateral sclerosis.
Low VEGFB and VEGFD gene expression is associated with early-stage non-small cell lung cancer.
Our study suggested that VEGF-B was an angiogenesis factor in vitro and that ERK1/2 and p38-related signaling pathways were involved in these VEGF-B activities.
VEGF-B has possible roles in cardiac protection, energy metabolism support, and neuroprotectin [review]
High VEGF-B levels might correlate with the presence of hyperlipidemia and target organ damage in type 2 diabetic patients.
High VEGFB expression is associated with bone marrow metastasis in neuroblastoma.
VEGF-B might be an important ligand in the signalling between the tumor and preexisting blood vessels to ensure a functional blood supply for tumor survival.
we report significant associations with overall survival and distant failure for certain VEGF(VEGF-B) family members.
Studies indicate that as a decoy VEGF receptor, aflibercept (VEGF-Trap) has binding affinity for VEGF-A, VEGF-B and placenta growth factor PGF.
VEGF and VEGFB counteractively regulate adipose development and function in energy metabolism.
VEGF-B is a potent regulator of the antioxidant pathway in retina.The antioxidant function of VEGF-B is mediated mainly by VEGFR1.
the expression and role of VEGF-B in diabetic corneal neuropathy was examined by using type 1 diabetic mice and cultured trigeminal ganglion (TG) neurons.
Data suggest that dietary fatty acids create epigenetic/nutrigenomic changes in methylation levels of CpG island at Vegfb promoter and changes in Vegfb expression in white adipocytes in vivo and in vitro, with particular up-regulation of DNA methylation by linoleic acid; Vegfb promoter methylation levels are closely related to Vegfb gene expression in visceral and subcutaneous adipose tissue.
PGC-1alpha is a master metabolic sensor that regulates the expression of Vegfa and Vegfb, coordinates blood vessels growth and fatty acid uptake with mitochondrial fatty acid oxidation.
These data therefore support a tightly controlled, paracrine signaling mechanism of VEGF-B to VEGFR1.
VEGFB-Induced Vascular Remodeling in Adipose Tissue Requires VEGF/VEGFR2. VEGFB-Induced Vascular Remodeling Improves Insulin Supply, Signaling, and Function in Obese Mice.
VEGF-B is dispensable for normal cardiac function under unstressed conditions and for high fat diet-induced metabolic changes.
VEGF-B is a vascular remodeling factor promoting cancer metastasis.
Data indicate that vascular endothelial growth factor B knockout (Vegf-b-/-) mice showed impaired nerve repair with concomitant impaired trophic function.
Data indicate that VEGF-B is a high-affinity VEGFR-1 ligand that, unlike PlGF, cannot efficiently induce signaling downstream of VEGFR-1.
results demonstrate that the vascular endothelium can function as an efficient barrier to excess muscle lipid uptake even under conditions of severe obesity and type 2 diabetes, and that this barrier can be maintained by inhibition of VEGF-B signalling
the RTEF-1-driven increase of VEGF-B plays an important role in communication between the endothelium and myocardium
Study indicates that VEGF-B, instead of acting as an angiogenic factor, exerts direct neuroprotective effects through FLT1.
Data show that no differences in vascular density, perfusion or immune cell infiltration upon altered Vegfb gene dosage were noted.
VEGF-B appears to be a coronary growth factor in rats but not in mice.
VEGF-B is involved in the retinal recovery processes and plays a potent role of neuroprotection in retinal ganglion cells after the optic nerve crush.
VEGF-B specifically controlled endothelial uptake of fatty acids via transcriptional regulation of vascular fatty acid transport proteins
Assignment of the mouse Vegfb gene to mouse chromosome 19 B
PCR-SSCP and DNA sequencing methods were applied to reveal 3 SNPs and a duplication in the bovine VEGF-B gene among 675 samples belonging to three native Chinese cattle breeds.
This gene encodes a member of the PDGF (platelet-derived growth factor)/VEGF (vascular endothelial growth factor) family. The VEGF family members regulate the formation of blood vessels and are involved in endothelial cell physiology. This member is a ligand for VEGFR-1 (vascular endothelial growth factor receptor 1) and NRP-1 (neuropilin-1). Studies in mice showed that this gene was co-expressed with nuclear-encoded mitochondrial genes and the encoded protein specifically controlled endothelial uptake of fatty acids. Alternatively spliced transcript variants encoding distinct isoforms have been identified.