User:JonSDSUGrad/Sandbox/TEST5 VEGFA

From Wikipedia, the free encyclopedia

vascular endothelial growth factor A
PDB rendering based on 1bj1.
Available structures: 1bj1, 1cz8, 1flt, 1kat, 1kmx, 1mjv, 1mkg, 1mkk, 1qty, 1tzh, 1tzi, 1vgh, 1vpf, 1vpp, 2fjg, 2fjh, 2vgh, 2vpf
Identifiers
Symbol(s)	VEGFA; MGC70609; VEGF; VEGF-A; VPF
External IDs	OMIM: 192240 MGI: 103178 HomoloGene: 2534
Gene ontology Molecular Function: • regulation of progression through cell cycle • angiogenesis • vasculogenesis • response to hypoxia • vascular endothelial growth factor receptor binding • proteinaceous extracellular matrix • extracellular space • cytoplasm • anti-apoptosis • signal transduction • multicellular organismal development • nervous system development • mesoderm development • growth factor activity • heparin binding • cell proliferation • membrane • cell migration • lung development • epithelial cell differentiation • positive regulation of vascular endothelial growth factor receptor signaling pathway • eye photoreceptor cell development • protein homodimerization activity • positive regulation of epithelial cell proliferation • extracellular matrix binding • induction of positive chemotaxis
Orthologs
	Human	Mouse
Entrez	7422	22339
Ensembl	ENSG00000112715	ENSMUSG00000023951
Uniprot	P15692	n/a
Refseq	NM_001025366 (mRNA) NP_001020537 (protein)	NM_001025250 (mRNA) NP_001020421 (protein)
Location	Chr 6: 43.85 - 43.86 Mb	Chr 17: 45.48 - 45.5 Mb
Pubmed search	[1]	[2]

[edit] Summary

This gene is a member of the PDGF/VEGF growth factor family and encodes a protein that is often found as a disulfide linked homodimer. This protein is a glycosylated mitogen that specifically acts on endothelial cells and has various effects, including mediating increased vascular permeability, inducing angiogenesis, vasculogenesis and endothelial cell growth, promoting cell migration, and inhibiting apoptosis. Elevated levels of this protein is linked to POEMS syndrome, also known as Crow-Fukase syndrome. Mutations in this gene have been associated with proliferative and nonproliferative diabetic retinopathy. Alternate transcriptional splice variants, encoding either freely secreted or cell-associated isoforms, have been characterized. There is also evidence for the use of non-AUG (CUG) translation initiation sites upstream of, and in-frame with the first AUG, leading to additional isoforms.