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. 2009 Apr;41(4):263–272. doi: 10.1093/abbs/gmp018

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© The Author 2009. Published by ABBS Editorial Office in association with Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.

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Fig. 2 — I-Smads mediate the crosstalk of the TGF-β signaling pathway with other pathways I-Smads could be transcriptionally induced by TGF-β/BMPs signaling and inhibit their signaling by negative feedback loops. Besides, they could also be induced by many other cytokines or stimuli, such as TNF-α/IL1, INF-γ, EGF, laminar shear stress, UV, TPA, etc. Smad7 has been reported to enhance the transcription of IκB, which is a key inhibitor of NF-κB signaling pathway. It may also disrupt the TRAF–TAK1–TAB2/3 complex, thus inhibiting NF-κB signaling. In addition, Smad7 was reported to down-regulate the protein level of β-catenin by recruitment of E3 ligase Smurf1. Smad7 itself could be degraded both in the nucleus and in the cytoplasm in proteasomal pathway.