Function
SMAD7 inhibits TGF-β signaling by preventing formation of Smad2/Smad4 complexes which initiate the TGF-β signaling. It interacts with activated TGF-β type I receptor therefore block the association, phosphorylation and activation of Smad2. By occupying type I receptors for Activin and bone morphogenetic protein (BMP), it also plays a role in negative feedback of these pathways.
Upon TGF- β treatment, Smad7 binds to discrete regions of Pellino-1 via distinct regions of the Smad MH2 domains. The interaction block formation of the IRAK1-mediated IL-1R/TLR signaling complex therefore abrogates NF-κB activity, which subsequently causes reduced expression of pro-inflammatory genes.
While Smad7 is induced by TGF-β, it is also induced by other stimuli, such as epidermal growth factor (EGF), interferon-γ and tumor necrosis factor (TNF)-α. Therefore it provides a cross-talk between TGF-β signaling and other cellular signaling pathways.
Read more about this topic: Mothers Against Decapentaplegic Homolog 7
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“Every boy was supposed to come into the world equipped with a father whose prime function was to be our father and show us how to be men. He can escape us, but we can never escape him. Present or absent, dead or alive, real or imagined, our father is the main man in our masculinity.”
—Frank Pittman (20th century)
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—Adam Phillips, British child psychoanalyst. “Worrying and Its Discontents,” in On Kissing, Tickling, and Being Bored, p. 58, Harvard University Press (1993)
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—Frank Pittman (20th century)