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Cristiano Simone

Researcher at University of Bari

Publications -  83
Citations -  13686

Cristiano Simone is an academic researcher from University of Bari. The author has contributed to research in topics: Cancer & Autophagy. The author has an hindex of 36, co-authored 73 publications receiving 11839 citations. Previous affiliations of Cristiano Simone include Temple University & Salk Institute for Biological Studies.

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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Journal ArticleDOI

p38 pathway targets SWI-SNF chromatin-remodeling complex to muscle-specific loci.

Cristiano Simone, +5 more
- 20 Jun 2004 - 
TL;DR: An unexpected function of differentiation-activated p38 is identified in converting external cues into chromatin modifications at discrete loci, by selectively targeting SWI-SNF to muscle-regulatory elements.
Journal ArticleDOI

Physical and Functional HAT/HDAC Interplay Regulates Protein Acetylation Balance

Alessia Peserico, +1 more
- 01 Jan 2011 - 
TL;DR: The identification of these complex networks of interacting proteins will likely foster the understanding of how cells regulate intracellular processes and respond to the extracellular environment and will offer the rationale for new therapeutic approaches based on epigenetic drugs in human diseases.
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Deacetylase inhibitors increase muscle cell size by promoting myoblast recruitment and fusion through induction of follistatin.

Simona Iezzi, +10 more
- 01 May 2004 - 
TL;DR: F follistatin is identified as a central mediator of the fusigenic effects exerted by deacetylase inhibitors on skeletal muscles and a rationale for their use to manipulate skeletal myogenesis and promote muscle regeneration is established.