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R-SMADs are receptor-regulatedSMADs. SMADs aretranscription factors that transduce extracellularTGF-β superfamily ligand signaling from cell membrane bound TGF-β receptors into the nucleus where they activate transcription TGF-β target genes. R-SMADS are directly phosphorylated on their c-terminus by type 1 TGF-β receptors through their intracellular kinase domain, leading to R-SMAD activation.[1]
R-SMADS includeSMAD2 andSMAD3 from the TGF-β/Activin/Nodal branch, andSMAD1,SMAD5 andSMAD9 from the BMP/GDP branch of TGF-β signaling.[1]
In response to signals by theTGF-β superfamily ofligands these proteins associate with receptorkinases and arephosphorylated at an SSXS motif at their extremeC-terminus. These proteins then typically bind to the common mediator Smad or co-SMADSMAD4.
Smad complexes then accumulate in thecell nucleus where they regulate transcription of specific target genes:
SMAD6 and SMAD7 may be referred to as I-SMADs (inhibitory SMADS), which form trimers with R-SMADS and block their ability to induce gene transcription by competing with R-SMADs for receptor binding and by marking TGF-β receptors for degradation.
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