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Downregulation of Ski and SnoN co-repressors by anisomycin.

Research paper by Aleida A Vázquez-Macías, Ana B AB Ruíz-Mendoza, Miguel A MA Fonseca-Sánchez, Marco A MA Briones-Orta, Marina M Macías-Silva

Indexed on: 22 Jun '05Published on: 22 Jun '05Published in: FEBS Letters



Abstract

Proteasome pathway regulates TGF-beta signaling; degradation of activated Smad2/3 and receptors turns TGF-beta signal off, while degradation of negative modulators such as Ski and SnoN maintains the signal. We have found that anisomycin is able to downregulate Ski and SnoN via proteasome as TGF-beta does, but through a mechanism independent of Smad activation. The mechanism used by anisomycin to downregulate Ski and SnoN is also independent of MAPK activation and protein synthesis inhibition. TGF-beta signal was the only pathway described causing Ski and SnoN degradation, thus this new effect of anisomycin on endogenous Ski and SnoN proteins suggests alternative processes to downregulate these negative modulators of TGF-beta signaling.