ALK2 (R206H), Active(A06-12BG)
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Description :Recombinant human ALK2 (R206H) (147-end) was expressed by baculovirus in Sf9 insect cells using an N-terminal GST tag.
Species :Human
Tag :GST tag
Expression System:Sf9 insect cells using baculovirus
Sequence :147-end (R206H)
Genbank Number :NM_001105
Specific Activity :Sample Kinase 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 :ALK2 belong to the transforming growth factor-beta (TGF-beta) superfamily of structurally related signaling proteins which encodes activin A type I receptor. ALK2 signals a particular transcriptional response in concert with activin type II receptors. Mutations in ALK2 are associated with fibrodysplasia ossificans progressiva (FOP) and the mutations are located in or adjacent to the GS regulatory region or active site of the kinase. The mutations in ALK2 were predicted by protein structure homology modeling to activate the ALK2 protein and enhance receptor signaling (1). Dysregulated ALK2 kinase activity plays a role in the pathogenesis of FOP (2).
References :
1. Kaplan, F. S.et.al:Classic and atypical fibrodysplasia ossificans progressiva (FOP) phenotypes are caused by mutations in the bone morphogenetic protein (BMP) type I receptor ACVR1. Hum. Mutat. 30: 379-390, 2009.
2. Yu, P. B.et.al: BMP type I receptor inhibition reduces heterotropic ossification. Nature Med. 14: 1363-1369, 2008.
Product Sheets (By Lot #) :
Research Areas :AKT/PKB Pathway, Angiogenesis, Cancer, Cardiovascular Disease, JAK/STAT Pathway, Neurobiology, Ser/Thr Kinases, Cancer, Neurobiology, Cardiovascular Disease, AKT/PKB Pathway, JAK/STAT Pathway, Angiogenesis, Ser/Thr Kinases