Human FLT1 Protein, Recombinant

产品货号：PR00296HuP1
   
$ 询价

规格    100ug

产品名称：Human FLT1 Protein, Recombinant
 
纯度：≥95 % as determined by SDS-PAGE
 
内毒素：/
 
生物活性：/
 
序列起止：Pro32~Thr421
 
标签：/
 
Uniprot链接：P17948
 
表达系统：E.coli
 
种属：Human
 
预测 N 端：Met
 
预测分子量：83.87 kDa
 
缓冲液：20mM Tris, 250mM imidazole, 500mM NaCl, pH8.0, containing 10% glycerol.
 
运输方式：This Protein is shipped as lyophilized powder at ambient temperature. Upon receipt, store it immediately at the temperature recommended.
 
稳定性 & 储存条件：Avoid repeated freeze/thaw cycles. Store at 2-8°C for one month. Aliquot and store at -80°C for 12 months.
 
复溶：Please refer to COA for detailed information
 
质量验证图：/

别称：Flt1, Fms-Related Tyrosine Kinase 1, Vascular Permeability Factor Receptor, Fms-like tyrosine kinase 1, Tyrosine-protein kinase receptor FLT
 
背景信息：VEGFR1/Flt-1. VEGFR1 (vascular endothelial growth factor receptor 1), also called Flt-1 (Fms-like tyrosine kinase), is a 180 kDa type I transmembrane glycoprotein in the class III subfamily of receptor tyrosine kinases (RTKs) (1, 2). While family members VEGFR1, VEGFR2/KDR/Flk-1 and VEGFR3/Flt-4 are all mainly expressed on endothelial cells and play central roles in vasculogenesis, angiogenesis, and lymphangiogenesis, only VEGFR1 is expressed on macrophages, and mainly plays inhibitory roles (1-3). VEGFR1 expression is also reported on osteoblasts, placental trophoblasts, renal mesangial cells, and some hematopoietic stem cells (1, 2). Like other class III RTKs, human VEGFR1 contains a signal peptide (aa 1-22), an extracellular domain (ECD aa 27-758) with seven Ig-like repeats, a transmembrane domain (aa 759-780) and a cytoplasmic region (aa 781-1338) with a tyrosine kinase domain and several autocatalytic phosphotyrosine sites. Human VEGFR1 ECD shares 78%, 78%, 84%, 87%, and 90% aa sequence identity with mouse, rat, porcine, canine and equine VEGFR1, respectively. Soluble forms of the VEGFR1 ECD are produced by alternative splicing, and may also be shed during regulated intracellular proteolysis (4-10). Both soluble and transmembrane forms can inhibit angiogenesis by binding and sequestering its ligands, VEGF (VEGF-A), VEGF-B or PlGF (6-11). VEGFR1 dimerizes upon ligand binding, which can include heterodimerization with VEGFR2 that modifies VEGFR2-mediated endothelial proliferation and vessel branching (8, 11, 12). VEGFR1 binds VEGF with higher affinity than does VEGFR2, but shows weaker kinase activity (9, 13). Both PlGF and VEGF induce autophosphorylation of transmembrane VEGFR1 (5, 9, 13). While deletion of mouse VEGFR1 is lethal due to overgrowth and disorganization of the vasculature, kinase-inactive mutants are viable (13, 14). VEGFR1 is upregulated during hypoxia, and participates in neovascularization and wound healing (1, 2, 15). VEGF R1 engagement on monocyte/macrophage lineage cells enhances their migration, and release of growth factors and cytokines (1, 3, 13, 16). Lymphangiogenesis, angiogenesis, and growth-promoting effects of VEGFR1 are thought to result from enhanced migration of macrophages from the bone marrow to tumors and tissues where they recruit endothelial progenitors (3, 16). Circulating levels of VEGFR1 increase during pregnancy and are further elevated in preeclampsia (4, 6, 17).

全称：Vascular endothelial growth factor receptor 1 (FLT1)

说明书：待上传