SMAD3, a receptor regulated SMAD (R-SMAD) is a transcriptional modulator activated by TGF-beta (transforming growth factor) and activin type 1 receptor kinase. SMAD3 is estimated to account for at least 80% of all TGF-beta-mediated response. Activated type I receptor phosphorylates receptor-activated SMADS (RSMADS) at their c-terminal two extreme serines in the SSXS motif. The phosphorylated R-SMAD translocate into nucleus, where they regulate transcription of target genes. SMAD3 signal transduction appears to be important in the rgulation of muscle-specific genes. Loss of SMAD3 is a feature of pediatric T-cell lymphoblastic leukemia, while upregulation of SMAD3 may be responsible for TGFB hyperresponsiveness observed in scleroderma.

HUMAN

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