ALK2 (R202I), Active(A06-12EG)
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Description :Recombinant human ALK2 (R202I) (147-end) was expressed by baculovirus in Sf9 insect cells using an N-terminal GST tag.
Tag :GST tag
Expression System:Sf9 insect cells using baculovirus
Sequence :147-end ((R202I)
Genbank Number :NM_001105
Specific Activity :Sample Activity Plot. For specific information on a given lot, see related technical data sheet.
Purity :Sample Purity Data. For specific information on a given lot, see related technical data sheet.
Storage, Stability, and Shipping :Store product at –70oC. For optimal storage, aliquot target into smaller quantities after centrifugation and store at recommended temperature. For most favorable performance, avoid repeated handling and multiple freeze/thaw cycles.
Applications :Kinase Assay
Molecular Weight :67 kDa
Gene Aliases :ACVR1, FOP, SKR1, TSRI, ACTRI, ACVR1A, ACVRLK2
Scientific Background :ALK 2 is a receptor serine/threonine kinase that is member of the ALK family and is upstream of signaling pathway involving the SMAD proteins especially SMAD1/5/8. Knockdown of ALK2, but not TGFβRI (ALK5), abrogates endoglin-mediated decrease in cell motility of prostate cancer cells and constitutively active ALK2 is sufficient to restore a low-motility phenotype in endoglin deficient cells (1). Therefore, endoglin decreases prostate cancer cell motility through activation of the ALK2-Smad1 pathway. ALK2 is the key gene involved in Fibrodysplasia ossificans progressiva (FOP), a rare autosomal dominant congenital disorder characterized by progressive heterotopic bone formation in muscle tissues (2).
1. Craft, C.S. et al: Endoglin inhibits prostate cancer motility via activation of the ALK2-Smad1 pathway. Oncogene. 2007 Nov 8;26(51):7240-50.
2. Shore, E. M. et al: A recurrent mutation in the BMP type I receptor ACVR1 causes inherited and sporadic fibrodysplasia ossificans progressiva. Nature Genet. 38: 525-527, 2006.
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Research Areas :AKT/PKB Pathway, Angiogenesis, Cancer, Cardiovascular Disease, JAK/STAT Pathway, Neurobiology, Ser/Thr Kinases