Transforming growth factor beta (TGFbeta) controls cellular behavior in 
embryonic and adult tissues. TGFbeta binding to serine/threonine kinase 
receptors on the plasma membrane activates Smad molecules and additional 
signaling proteins that together regulate gene expression. In this review, 
mechanisms and models that aim at explaining the coordination between several 
components of the signaling network downstream of TGFbeta are presented. We 
discuss how the activity and duration of TGFbeta receptor/Smad signaling can be 
regulated by post-translational modifications that affect the stability of key 
proteins in the pathway. We highlight links between these mechanisms and human 
diseases, such as tissue fibrosis and cancer.