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. 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.
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Fibrodysplasia ossificans progressiva (FOP) is a rare autosomal dominant disorder of skeletal malformations and progressive extraskeletal ossification. We mapped FOP to chromosome 2q23-24 by linkage analysis and identified an identical heterozygous mutation (617G --> A; R206H) in the glycine-serine (GS)
Endoglin is a transforming growth factor beta (TGFbeta) superfamily auxiliary receptor. We had previously shown that it suppressed prostate cancer (PCa) cell motility, and that its expression was lost during PCa progression. The mechanism by which endoglin inhibits PCa cell
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