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lüll Phospho-control of TGF-beta superfamily signaling Wrighton KH; Lin X; Feng XHCell Res 2009[Jan]; 19 (1): 8-20Members of the transforming growth factor-beta (TGF-beta) family control a broad range of cellular responses in metazoan organisms via autocrine, paracrine, and endocrine modes. Thus, aberrant TGF-beta signaling can play a key role in the pathogenesis of several diseases, including cancer. TGF-beta signaling pathways are activated by a short phospho-cascade, from receptor phosphorylation to the subsequent phosphorylation and activation of downstream signal transducers called R-Smads. R-Smad phosphorylation state determines Smad complex assembly/disassembly, nuclear import/export, transcriptional activity and stability, and is thus the most critical event in TGF-beta signaling. Dephosphorylation of R-Smads by specific phosphatases prevents or terminates TGF-beta signaling, highlighting the need to consider Smad (de)phosphorylation as a tightly controlled and dynamic event. This article illustrates the essential roles of reversible phosphorylation in controlling the strength and duration of TGF-beta signaling and the ensuing physiological responses.|*Signal Transduction[MESH]|Animals[MESH]|Phosphorylation[MESH]|Receptors, Transforming Growth Factor beta/*metabolism[MESH]|Smad Proteins/physiology[MESH]|Transcription, Genetic[MESH]|Transforming Growth Factor beta/*physiology[MESH]|Ubiquitin/metabolism[MESH] |