Overview:

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).

References:

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