The transforming growth factor β (TGFβ)/activin/BMP family of growth factors plays a diverse and important role in growth, development, and differentiation. These growth factors act through their binding to heteromeric plasma membrane receptor protein kinases which, upon ligand binding, become activated and trigger an intracellular signaling cascade. Specifically, receptor activation induces the translocation of a set of conserved proteins named Smads (Sma- and Mad-related proteins) to the nucleus, resulting in gene activation. Smad2 is a ubiquitously expressed protein of 58 kDa that is phosphorylated and translocated to the nucleus in response to TGFβ, but not BMP. The overall response to TGFβ is growth inhibition. The Smad2 gene is located in chromosome 18q21.1 which is often absent in several human cancers. Furthermore, some missense mutations on the Smad2 gene were identified in colorectal carcinomas, suggesting Smad2 may function as a tumor suppressor in normal cells.
Investigators should note that potential crossreactivity to Smad3 is predicted based on sequence homology of the immunogen, Mouse Smad2 aa. 142-263. In addition, reactivity to mouse Smad2, using siRNA knockdown, has recently been described (Dzwonek et al.). Reactivity to canine Smad3 has also been reported using nuclear extracts (Lehman et al.).