Recombinant Human VEGF165 (Active) protein is a Human Fragment protein, in the 27 to 191 aa range, expressed in HEK 293, with >95% purity and < 1 EU/µg endotoxin level.
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N-VEGF. Participates in the induction of key genes involved in the response to hypoxia and in the induction of angiogenesis such as HIF1A (PubMed:35455969). Involved in protecting cells from hypoxia-mediated cell death (By similarity). VEGFA. Growth factor active in angiogenesis, vasculogenesis and endothelial cell growth (PubMed:34530889). Induces endothelial cell proliferation, promotes cell migration, inhibits apoptosis and induces permeabilization of blood vessels. Binds to the FLT1/VEGFR1 and KDR/VEGFR2 receptors, heparan sulfate and heparin. Binds to the NRP1/neuropilin-1 receptor. Binding to NRP1 initiates a signaling pathway needed for motor neuron axon guidance and cell body migration, including for the caudal migration of facial motor neurons from rhombomere 4 to rhombomere 6 during embryonic development (By similarity). Also binds the DEAR/FBXW7-AS1 receptor (PubMed:17446437). Isoform VEGF165B. Binds to the KDR receptor but does not activate downstream signaling pathways, does not activate angiogenesis and inhibits tumor growth.
VEGF, VEGFA, L-VEGF, Vascular permeability factor, VPF
Recombinant Human VEGF165 (Active) protein is a Human Fragment protein, in the 27 to 191 aa range, expressed in HEK 293, with >95% purity and < 1 EU/µg endotoxin level.
Constituents: 91.99% PBS, 8% Trehalose
N-VEGF
Belongs to the PDGF/VEGF growth factor family.
Vascular endothelial growth factor A, long form
This product is an active protein and may elicit a biological response in vivo, handle with caution.
Vascular endothelial growth factor A (VEGFA) also known as VEGF or vascular permeability factor (VPF) is a protein that plays a central role in angiogenesis as well as in the growth of blood vessels. The molecular weight of VEGFA varies depending on the isoform typically ranging from 34 to 42 kDa. VEGFA is expressed in many tissues including fibroblasts macrophages endothelial cells and platelets. Its expression levels can increase in response to stimuli like hypoxia or inflammatory cytokines. VEGFA is an important target in research for therapies related to vascular diseases and cancer.
VEGFA functions by promoting the proliferation and migration of vascular endothelial cells. It operates both as a homodimer and as part of complex signaling cascades interacting with VEGF receptors on cell surfaces to trigger downstream signals for angiogenesis. This includes endothelial cell growth migration and the new blood vessel formation process. VEGFA's activity is important for physiological processes such as wound healing and embryonic development and it also contributes to pathological conditions through its unregulated expression in diseases.
Many processes involve VEGFA including the PI3K/AKT pathway and the MAPK/ERK pathway. These pathways regulate cell survival growth and differentiation. Other proteins like PLGF (placenta growth factor) and VEGFB often accompany VEGFA in these pathways aiding in distinct but overlapping roles. These interactions are transmitted through binding to VEGF receptors such as VEGFR-1 and VEGFR-2 subsequently activating various signaling cascades necessary for cellular and tissue homeostasis.
VEGFA relates to cancer and age-related macular degeneration among others. In cancer overexpression of VEGFA can lead to excessive angiogenesis supplying blood to tumors and facilitating tumor growth. In age-related macular degeneration upregulation of VEGFA contributes to the progression of the disease by promoting the formation of abnormal blood vessels under the retina. Anti-VEGFA therapies such as anti-VEGF antibodies (e.g. bevacizumab) can target these overexpressed pathways. VEGFA interacts with other proteins like HIF-1α which regulates its expression under hypoxia a common condition in tumors.
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