Human ALK-1, His Tag (AL1-H5227) is expressed from human 293 cells (HEK293). It contains AA Asp 22 - Gln 118 (Accession # NP_000011.2).
Predicted N-terminus: Asp 22
This protein carries a polyhistidine tag at the C-terminus.
The protein has a calculated MW of 11.5 kDa. The protein migrates as 22-28 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.
Less than 1.0 EU per μg by the LAL method.
>97% as determined by SDS-PAGE.
Lyophilized from 0.22 μm filtered solution in PBS, pH7.4. Normally trehalose is added as protectant before lyophilization.
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Please see Certificate of Analysis for specific instructions.
For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.
For long term storage, the product should be stored at lyophilized state at -20°C or lower.
Please avoid repeated freeze-thaw cycles.
This product is stable after storage at:
- -20°C to -70°C for 12 months in lyophilized state;
- -70°C for 3 months under sterile conditions after reconstitution.
Human ALK-1, His Tag on SDS-PAGE under reducing (R) condition. The gel was stained overnight with Coomassie Blue. The purity of the protein is greater than 97%.
Serine/threonine-protein kinase receptor R3 is an enzyme that in humans is encoded by the ALK1 gene. ALK1 is a receptor in the TGF beta signaling pathway. ALK1 protein is a receptor in the TGF beta signaling pathway. It plays an important role in vascular development, remodeling, and pathologic angiogenesis, play a role in stabilizing angiogenic vessels and contribute to resistance to anti-VEGF therapies, ALK1 blockade may represent an effective therapeutic opportunity complementary to the current antiangiogenic modalities in the clinic. Recently, researcher found that, ALK1-Fc inhibited BMP9-mediated Id-1 expression in human umbilical vein endothelial cells and inhibited cord formation by these cells on a Matrigel substrate, in a chick chorioallantoic membrane assay, ALK1-Fc reduced vascular endothelial growth factor-, fibroblast growth factor-, and BMP10-mediated vessel formation, and ALK1-Fc treatment reduced tumor burden in mice receiving orthotopic grafts of MCF7 mammary adenocarcinoma cells.