Introduction To VEGFA
Drug targets a biomolecule that can directly bind to drugs and then react. Generally, the target refers to a protein related to the cause of disease. The focus of the target began with focusing on tumors and then began to spread to various fields. Introduction to the VEGFA domain is a common target in medicine.
VEGFA (or VEGF) is a prototype member of a family that also includes the placental growth factor (PL GF, also known as PGF), VE GF B, VE GF C, and VEGFD. The molecular weight of VEGF by SDS-PAGE and 23-kDa under nonreduced conditions is consistent with the homodimer. Indeed, most normal and abnormal cells can produce VEGF. In adults, VEGF induces the proliferation, budding, migration, and tube formation of ECs, and is a potent survival factor for ECs during physiology and growth.
Function of Target VEGFA
Promote the secretion of VEGF-A by microglia, increase the proliferation and migration of vascular endothelial cells through the PI3K / AKT / Bcl-2 pathway, and inhibit microglial cell apoptosis. Many studies have shown that VEGF has multiple roles in skeletal development, promoting vascularization during fetal skeletogenesis, and regulating the survival and activity of chondrocytes and osteoblasts. VEGF plays a role not only in mediating bone vascularization, but also in allowing the normal differentiation of hypertrophic chondrocytes, osteoblasts, EC, and osteoclasts. The hypoxic tumor microenvironment (TME) is driven by the transcriptional activity of HIF, and HIF can upregulate VEGFA to induce tumor angiogenesis, which is a key marker of cancer progression.
Gene Pathway of Target VEGFA
Phospholipase Cc-extracellular regulatory kinase pathway phospholipase Cc (PLCc) is an important mediator of VEGFR 2-dependent proliferation. An alternative pathway of Src activation involves binding to Y1059 in the VEGFR 2 kinase domain or to the scaffolding proteins Gab 1 and Gab 2. Src family kinases can phosphorylate, thereby activating receptor tyrosine kinases to initiate downstream signaling in a ligand-independent manner. The Src family kinases phosphorylate the vascular endothelial cadherin (VE-cadherin) in adherens junctions, resulting in elevated vascular permeability. Hypoxia can activate a variety of RAS effector pathways, including extracellular signal-regulated kinase, JUN N terminal kinase (JNK), p38, mitogen-activated protein kinase (MAPK), protein kinase B (PKB, also known as AKT), and RHO 61. AKT is a major downstream target of phosphoinositide 3 kinase (PI3K), and inhibition of PI3K strongly downregulates hypoxia induction of VEGF62. Activated RAS can also control VE GF protein activity by stimulating the expression of several proteases (including MMP), and MMP activates VEGF protein secretion to increase its extracellular levels.

Fig 1: VEGFA Gene Pathway. (Reference source: Claesson-Welsh L, Welsh M. VEGFA and tumor angiogenesis. J Intern Med. 2013 Feb;273(2):114-27. )
Alpha Lifetech Can Provide
Currently, various immune drugs targeting VEGFA targets are in the updating iteration, and taking the disease alone or in combination with other products has become a new approach with remarkable achievements. The VEGFA targets have shown important research value and application prospects in both biology and drug research and development. With further research and detection technology advances, VEGFA target products are also essential in medical research. Alpha Lifetech can provide VEGFA with corresponding products and help each customer's research and development. In addition, Alpha Lifetech also provides advanced expression systems and purification services to accelerate antibody research and development. Our synthesized antibody expression undergoes rigorous quality validation, including sequencing validation and functional expression analysis, to ensure high fidelity and performance. In addition, Alpha Lifetech provides customized solutions for recombinant proteins, such as codon optimization, promoter selection, and vector design, supplemented by downstream applications such as protein expression analysis to meet specific experimental needs.
| Catalog Number | Product Name | Product Sizes |
|---|---|---|
| ADT1236 | 1mg,5mg | |
| ADT1689 | 1mg,5mg | |
| ADT1172 | 1mg,5mg | |
| ADT1428 | 1mg,5mg | |
| ADT1300 | 1mg,5mg | |
| ADT1020 | 100ug,1mg,5mg | |
| ADT1460 | 100ug,1mg,5mg | |
| ADT1697 | 1mg,5mg | |
| ADT1018 | 1mg,5mg | |
| ADT1090 | 1mg,5mg | |
| ADT1106 | 1mg,5mg | |
| ADT1309 | 1mg,5mg | |
| ADT1535 | 100ug,1mg,5mg | |
| ADT1691 | 100ug,1mg,5mg | |
Reference
[1] Claesson-Welsh L, Welsh M. VEGFA, and tumor angiogenesis. J Intern Med. 2013 Feb;273(2):114-27.
[2] Zou G, Zhang X, Wang L, Li X, Xie T, Zhao J, Yan J, Wang L, Ye H, Jiao S, Xiang R, Shi Y. Herb-sourced emodin inhibits angiogenesis of breast cancer by targeting VEGFA transcription. Theranostics. 2020 May 22;10(15):6839-6853.
[3] White AL, Bix GJ. VEGFA Isoforms as Pro-Angiogenic Therapeutics for Cerebrovascular Diseases. Biomolecules. 2023 Apr 20;13(4):702.
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2018-07-16


