protein

VEGFR-1 Protein, Mouse (HEK293, His)

HY-P73553

2 μg;10 μg

36;100 USD

VEGFR-1 Protein, Mouse (HEK293, His)

proteins

HEK293

2 μg;10 μg

36;100 USD

The VEGFR-1 protein is a key tyrosine protein kinase receptor. VEGFR-1 Protein, Mouse (HEK293, His) is the recombinant mouse-derived VEGFR-1 protein, expressed by HEK293 , with C-His, C-10*His labeled tag. The total length of VEGFR-1 Protein, Mouse (HEK293, His) is 737 a.a., with molecular weight of ~130 kDa.

Mouse

VEGFR-1, a tyrosine-protein kinase, acts as a pivotal cell-surface receptor for VEGFA, VEGFB, and PGF, playing indispensable roles in embryonic vasculature development, angiogenesis regulation, cell survival, migration, macrophage function, chemotaxis, and cancer cell invasion. It functions as a positive regulator in the regression of postnatal retinal hyaloid vessels. While potentially acting as a negative regulator of embryonic angiogenesis by curbing excessive endothelial cell proliferation, VEGFR-1 also exhibits cell-type-specific promotion of proliferation, survival, and angiogenesis in adulthood, especially in response to PGF. With a high affinity for VEGFA, it modulates KDR signaling through heterodimer formation. Acting as a potential negative regulator of VEGFA signaling, it limits free VEGFA, hindering its binding to KDR. Ligand binding triggers various signaling cascades, including PLCG activation, leading to diacylglycerol and inositol 1,4,5-trisphosphate production, as well as protein kinase C activation. Additionally, VEGFR-1 mediates the phosphorylation of PIK3R1, initiating the phosphatidylinositol 3-kinase pathway, and activates MAPK1/ERK2, MAPK3/ERK1, and AKT1 signaling pathways. It also phosphorylates SRC, YES1, PLCG, and potentially CBL, facilitating the phosphorylation of AKT1 and PTK2/FAK1.

Vascular endothelial growth factor receptor 1; FLT; FLT1; FRT; VEGFR-1

Greater than 90% as determined by reducing SDS-PAGE.

Lyophilized from a 0.2 μm filtered solution of PBS, pH 7.4.

Room temperature in continental US; may vary elsewhere.