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Description :Rabbit Polyclonal Antibody
Specificity :Recognizes the ALK2 protein
Cited Applications :WB, ELISA
Cross Reactivity :Human and Mouse
Host / Isotype / Clone# :Rabbit, IgG
Immunogen :ALK2 antibody was raised against a 14 amino acid synthetic peptide near the amino terminus of the human ALK2
Purification :Affinity chromatography
Stability :Store at 4oC (add 0.1% NaN3) for several months, and at -20oC for longer periods. 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.
Sample Data :Western blot analysis of ALK2 in A549 cell lysate with ALK2 antibody at 1 ug/ml in (A) the absence and (B) the presence of blocking peptide.
Scientific Background :ALK2 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, Cancer, Cardiovascular Disease, AKT/PKB Pathway, JAK/STAT Pathway, Angiogenesis, Ser/Thr Kinases