I-SMAD competes with SMAD2/3 for type I receptor (TGFBR1)

Stable Identifier
Reaction [binding]
Homo sapiens
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I-SMADs (SMAD6 and SMAD7) reside in the nucleus presumably to be sequestered from the TGF-beta receptor complex and thus avoid inappropriate silencing of the signaling pathway. Upon activation of the signaling pathway, I-SMADs exit the nucleus and are recruited to the signaling TGF-beta receptor complex. I-SMADs directly bind to the so-called L45 loop of the type I receptor, the site of binding of R-SMADs. Thus, I-SMADs competitively inhibit the activation/phosphorylation of R-SMADs.

Literature References
PubMed ID Title Journal Year
9335507 Identification of Smad7, a TGFbeta-inducible antagonist of TGF-beta signalling

Nakao, A, Afrakhte, M, Moren, A, Nakayama, T, Christian, JL, Heuchel, R, Itoh, S, Kawabata, M, Heldin, NE, Heldin, CH, ten Dijke, P

Nature 1997
9215638 The MAD-related protein Smad7 associates with the TGFbeta receptor and functions as an antagonist of TGFbeta signaling

Hayashi, H, Abdollah, S, Qiu, Y, Cai, J, Xu, YY, Grinnell, BW, Richardson, MA, Topper, JN, Gimbrone MA, Jr, Wrana, JL, Falb, D

Cell 1997
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Event Information
Orthologous Events