Expert Reviews in Molecular Medicine: http://www.expertreviews.org/
Accession information: Vol. 7; Issue 29; 20 December 2005 Abstract
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JAK–STAT and Smad signalling cascades

Beverley Wilkinson, Jocelyn S. Downey and Christopher E. Rudd

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Figure 4. JAK–STAT and Smad signalling cascades. (a) Cytokine signalling via JAKs and STATs. Binding of cytokines to cytokine receptors leads to the activation of JAKs, which phosphorylate STAT transcription factors. Phosphorylation of STATs allows them to dimerise and translocate to the nucleus where they activate gene transcription. (b) TGF-b-receptor-mediated signalling via Smads. The TGF-b receptor comprises heterodimeric transmembrane serine/threonine kinases consisting of type I and type II receptor chains. Phosphorylated type I TGF-b receptors bind and phosphorylate the receptor-regulated Smads (R-Smads): Smad2 and Smad3. Once phosphorylated, the R-Smads dissociate from the receptor complex, form homotrimers, and bind to Smad4, the common mediator Smad (Co-Smad). The R-Smad–Co-Smad complex translocates into the nucleus and regulates gene transcription by interacting with tissue-specific transcriptional co-activators or co-repressors. Smad7 interferes with the phosphorylation of Smad2 and 3 phosphorylation. Abbreviations: JAK, Janus kinase; STAT, signal transducer and activators of transcription; TGF-b, transforming growth factor b.

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