Sirt1 interaction with active Smad2 modulates transforming growth factor-β regulated transcription.

ABSTRACT:

Background

The simplicity of Transforming Growth Factor ß (TGFβ) signaling pathway, linear and non-amplified, hardly sustains its variety of responses. This is often justified by the complex regulation showed by Smad proteins, TGFβ signaling intracellular transducers, object of post-translational modifications that modulate TGFβ-dependent transcription. Protein acetylation is emerging as a compelling mechanism affecting the activities of significant transcription factors, including p53, FOXO or NF-kB. Smad proteins might be controlled by this mechanism, implying that accessory factors capable of altering Smads-transcriptional complexes acetylation status and hence regulate TGFβ responses remain to be identified. Understanding this interaction may help in the assessment of TGFβ sign

SUBMITTER: Garcia-Vizcaino EM 

PROVIDER: S-EPMC5706420 | biostudies-literature | 2017 Nov

REPOSITORIES: biostudies-literature