Recombinant human ALK2 (147–end) was expressed by baculovirus in Sf9 insect cells using an N-terminal GST tag. 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).
ADP-Glo™ Kinase Assay is a luminescent kinase assay that measures ADP formed from a kinase reaction; ADP is converted into ATP, which is a substrate in a reaction catalyzed by Ultra-Glo™ Luciferase that produces light. The luminescent signal positively correlates with ADP amount and kinase activity. The assay is well suited for measuring the effects chemical compounds have on the activity of a broad range of purified kinases, making it ideal for both primary screening as well as kinase selectivity profiling. The ADP-Glo™ Kinase Assay can be used to monitor the activity of virtually any ADP-generating enzyme (e.g., kinase or ATPase) using up to 1mM ATP.
Profile More Compounds In-House: ADP-Glo™ Kinase Assay + Kinase Enzyme System is optimized so that you are up and running in no time. Complete Systems: The Kinase Enzyme Systems include a recombinant kinase enzyme, a substrate appropriate for the enzyme, a reaction buffer, DTT and supplemental reagents as needed. Obtain Reliable Results: The broad dynamic range, the ease of use and better sensitivity obtained with ADP-Glo™ Kinase Assay result in less ambiguous data.
Notes
Kinase Enzyme System manufactured by SignalChem.
Bulk quantities available upon request.
References
1.Craft, C.S. et al. (2007) Endoglin inhibits prostate cancer motility via activation of the ALK2-Smad1 pathway. Oncogene 26, 7240–50.
2.Shore, E.M. et al. (2006) A recurrent mutation in the BMP type I receptor ACVR1 causes inherited and sporadic fibrodysplasia ossificans progressiva. Nature Genet. 38, 525–7.