Research ArticleCell Biology

Inflammatory stimuli induce inhibitory S-nitrosylation of the deacetylase SIRT1 to increase acetylation and activation of p53 and p65

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Science Signaling  11 Nov 2014:
Vol. 7, Issue 351, pp. ra106
DOI: 10.1126/scisignal.2005375

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  • Correction to references in the Research Article “Inflammatory stimuli induce inhibitory S-nitrosylation of the deacetylase SIRT1 to increase acetylation and activation of p53 and p65”

    The Editors wish to notify readers that multiple references were cited incorrectly and have been revised for accuracy in the Research Article “Inflammatory stimuli induce inhibitory S-nitrosylation of the deacetylase SIRT1 to increase acetylation and activation of p53 and p65” by Shinozaki et al. This was corrected on 21 November 2014.

    Competing Interests: None declared.
  • The functional importance of SIRT-1 is context-dependent
    • RANJEET SINGH MAHLA, Ph.D. student, Indian Institute of Science Education and Research Bhopal, India

    Shinozaki et al. (2014) have demonstrated that SIRT-1 and NF-kB regulate each other, where S-nitrosylation of SIRT1 is central for transcriptional regulation of p53 and p65 and action of iNOS and nNOS for inflammatory outcomes. However, the study has ignored the functional importance of other deacetylases (sirutins and HDACs) involved in transcriptional regulation of diverse genes of apoptotic signaling pathways. Can the author address why SIRT-1 is conceptualized as central to inflammatory outcomes. The 2014 study by Ren et al.  (doi: 10.1128/JVI.02861-13) has shown that SIRT-1 targets c-Jun of the AP1 complex in HBV infection. So, is it possible that the SIRT-1 role in inflammation is context-dependent, such as in infection or age-related disorders? 

    Competing Interests: None declared.

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