- 1. hSMAD6
- [Encoded by MADH6 Gene (SMAD Family), ubiquitous (predominantly vascular endothelium) SMAD6 Protein Isoforms A (496-aa 53.5-kD) and B (235-aa) act similar to other MAD-proteins as second messengers distal to TGFBRs and contain an N-terminal DWA/MH1 domain and a C-terminal DWB/MH2 domain. An inhibitory SMAD phosphorylated by type 1 receptor kinase, SMAD6 acts as an antagonist of TGF-beta type 1 receptor signaling. A selective inhibitor of BMPs signaling; SMAD6 competes with SMAD4 for receptor-activated SMAD1. SMAD6 interacts with TGF-beta type I receptor superfamily members, SMAD1, HOXC8, and HOXC9. MADH6 and MADH7 form complexes. (from LocusLink, Swiss-Prot, OMIM, and NCI) ( NCI )] (UMLS (NCI) C0540682) =Amino Acid, Peptide, or Protein; Biologically Active Substance ;
| - 2. hSMAD7
- [Encoded by MADH7 Gene (SMAD Family) and induced by TGF-beta and IFNG, ubiquitous (lung, vascular endothelium highest) 426-amino acid SMAD7 Protein is an inhibitory Activin/TGFBR1 signaling component containing DWA/MH1 and DWB/MH2 domains. SMAD7 lacks C-terminal phosphorylation sites of other MAD proteins, suggesting distinct regulation. Adaptor SMAD7 constitutively recruits nuclear E3 ubiquitin ligase SMURF2 to TGFBR complexes preventing SMAD2 access and causing proteasomal and lysosomal receptor degradation. SMAD7-expressing cells are susceptible to apoptosis induced by TGFB, TNFA, serum withdrawal, or loss of cell adhesion. SMAD7 decreases NFKB activity, promoting apoptosis. RAS suppresses SMAD7 inhibition of NFKB and potentiation of apoptosis. MADH7 and MADH6 form complexes. (from LocusLink, Swiss-Prot, OMIM, and NCI) ( NCI )] (UMLS (NCI) C0664910) =Amino Acid, Peptide, or Protein; Biologically Active Substance ;
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