A nitric oxide-dependent cross-talk between class i and III histone deacetylases accelerates skin repair

Francesco Spallotta, Chiara Cencioni, Stefania Straino, Simona Nanni, Jessica Rosati, Simona Artuso, Isabella Manni, Claudia Colussi, Giulia Piaggio, Fabio Martelli, Sergio Valente, Antonello Mai, Maurizio C. Capogrossi, Antonella Farsetti, Carlo Gaetano

Research output: Contribution to journalArticlepeer-review

Abstract

Background: Nitric oxide (NO) regulates class I and IIa histone deacetylase (HDAC) function. NO production is regulated by class III HDACs (sirtuins). Results: NO functions as a bridging molecule between class I and sirtuins (SIRTs). Conclusion: The SIRT-NO-class I HDAC axis provides key signals during wound repair. Significance: Modulation of HDAC activity may play an important role in tissue regeneration.

Original languageEnglish
Pages (from-to)11004-11012
Number of pages9
JournalJournal of Biological Chemistry
Volume288
Issue number16
DOIs
Publication statusPublished - Apr 19 2013

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Molecular Biology

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