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Your Position: ホーム > Protein > ALK-1 > AL1-H5228

Human ALK-1 / ACVRL1 Protein, His Tag

  • Synonym
    ACVRL1,ACVRLK1,ALK-1,HHT,HHT2,ORW2,SKR3,TSR-I
  • Source
    Human ALK-1, His Tag(AL1-H5228) is expressed from human 293 cells (HEK293). It contains AA Asp 22 - Gln 118 (Accession # P37023).
    Predicted N-terminus: Asp 22
  • Molecular Characterization
    ALK-1 Structure

    This protein carries a polyhistidine tag at the C-terminus

    The protein has a calculated MW of 12.6 kDa. The protein migrates as 23-28 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.

  • Endotoxin
    Less than 1.0 EU per μg by the LAL method.
  • Purity

    >90% as determined by SDS-PAGE.

  • Formulation

    Lyophilized from 0.22 μm filtered solution in PBS, pH7.4 with trehalose as protectant.

    Contact us for customized product form or formulation.

  • Reconstitution

    Please see Certificate of Analysis for specific instructions.

    For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.

  • Storage

    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:

    1. -20°C to -70°C for 12 months in lyophilized state;
    2. -70°C for 3 months under sterile conditions after reconstitution.
SDS-PAGE
ALK-1 SDS-PAGE

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 90%.

  • Background
    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.
  • Clinical and Translational Updates

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