protein

ACVRL1/ALK1 Protein, Mouse (HEK293, His-Fc)

HY-P72819

10 μg;50 μg;100 μg

145;375;600 USD

ACVRL1/ALK1 Protein, Mouse (HEK293, His-Fc)

proteins

HEK293

10 μg;50 μg;100 μg

145;375;600 USD

ALK-1, also known as ACVRL1, is a type I receptor for TGF-β superfamily with 2 ligands, BMP9 and BMP10. ALK-1 is predominantly expressed in endothelial cells and plays a critical role in regulating developmental and pathological angiogenesis [1] [2] . ACVRL1/ALK1 Protein, Mouse (HEK293, His-Fc) is produced in HEK293 cells with a C-Terminal His-tag and a C-Terminal Fc-tag. It consists of 119 amino acids (M1-P119).

Mouse

ALK-1, also known as ACVRL1, is a type I receptor for TGF-β superfamily with 2 ligands, BMP9 and BMP10. ALK-1 is predominantly expressed in endothelial cells and plays a critical role in regulating angiogenesis [1] [2] . Mature human ALK-1 shares 89% amino acid sequence identity with mouse and rat ALK-1. While, mouse ALK-1 shares 96% aa sequence identity with rat ALK-1 protein. ALK-1 is able to bind to TGF-β1 or activins in the presence of either TβR-II or activin type II receptors, respectively. However, ALK-1 does not elicit a specific transcriptional response. Thus, ALK-1 has been considered an “orphan” receptor. ALK-1 is a type I receptor that mediates signaling of BMP9 (bone morphogenetic protein) and BMP10, proteins in the TGF-β superfamily. Signaling through ALK-1 results in phosphorylation of the intracellular Smad 1/5/8 cascade which activates proangiogenic transcription factors such as ID1 and ID3. ALK-1 binds to TGF-β1 and phosphorylates Smad1 and Smad5. Overexpression of ALK-1 in HepG2 cells inhibits the ALK5-mediated TGF-β1 response. The balance between ALK-1 and ALK5 may be crucial for controlling the properties of endothelium during angiogenesis [1] . BMP9/BMP10/ALK-1 signaling controlled the specific gene expression program and survival of Kupffer cells (KCs) through a Smad4-dependent pathway. Functionally, the loss of ALK-1 resulted in impaired capture of L. monocytogenes and overwhelming disseminated infections [2] . ALK-1 is expressed in blood vessels during embryogenesis and adult stages. In addition, mutations of the ALK-1 gene have been linked to the type II hereditary hemorrhagic telangiectasia [1] . ALK-1 inhibits BMP9-mediated Id-1 expression in human umbilical vein endothelial cells. In a chick chorioallantoic membrane assay, ALK-1 reduces VEGF-, FGF-, and BMP10-mediated vessel formation. In addition, ALK1 reduces tumor burden in mice receiving orthotopic grafts of MCF7 mammary adenocarcinoma cells [3] .

Serine/threonine-protein kinase receptor R3; SKR3; ALK-1; TSR-I; ACVRL1

Greater than 95% as determined by reducing SDS-PAGE

Supplied as a 0.2 μm filtered solution of PBS, pH 7.4.

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