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R-SMADs are receptor-regulated SMADs. SMADs are transcription factors that transduce extracellular TGF-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. R-SMADS include SMAD2 and SMAD3 from the TGF-β/Activin/Nodal branch, and SMAD1, SMAD5 and SMAD8 from the BMP/GDP branch of TGF-β signaling. R-SMADs include SMAD1, SMAD2, SMAD3, SMAD5, and SMAD8. In response to signals by the TGF-β superfamily of ligands these proteins associate with receptor kinases and are phosphorylated at an SSXS motif at their extreme C-terminus. These proteins then typically bind to the common mediator Smad or co-SMAD SMAD4. Smad complexes then accumulate in the cell nucleus where they regulate transcription of specific target genes: * SMAD2 and SMAD3 are activated in response to TGF-β/Activin or Nodal signals. * SMAD1, SMAD5 and SMAD8 are activated in response to BMPs bone morphogenetic protein or GDP signals. 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. ==References== 抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』 ■ウィキペディアで「R-SMAD」の詳細全文を読む スポンサード リンク
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