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Paolo Salomoni

Researcher at German Center for Neurodegenerative Diseases

Publications -  128
Citations -  19423

Paolo Salomoni is an academic researcher from German Center for Neurodegenerative Diseases. The author has contributed to research in topics: Promyelocytic leukemia protein & Stem cell. The author has an hindex of 51, co-authored 124 publications receiving 17318 citations. Previous affiliations of Paolo Salomoni include University of Modena and Reggio Emilia & University of Milan.

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Journal ArticleDOI

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

The transcriptional role of PML and the nuclear body

Sue Zhong, +2 more
- 01 May 2000 - 
TL;DR: The current understanding of the biological functions of PML and the nuclear body is summarized, and a role for these intra-nuclear structures in the regulation of transcription is discussed.
Journal ArticleDOI

The Role of PML in Tumor Suppression

Paolo Salomoni, +1 more
- 25 Jan 2002 - 
TL;DR: The PML gene, involved in the t(15;17) chromosomal translocation of acute promyelocytic leukemia (APL), encodes a protein which localizes to the PML-nuclear body, a subnuclear macromolecular structure, which controls apoptosis, cell proliferation, and senescence.
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Targeting autophagy potentiates tyrosine kinase inhibitor-induced cell death in Philadelphia chromosome-positive cells, including primary CML stem cells.

Cristian Bellodi, +20 more
- 01 May 2009 - 
TL;DR: The authors showed that IM-induced autophagy did not involve c-Abl or Bcl-2 activity, but was associated with ER stress and was suppressed by depletion of intracellular Ca2+, suggesting it is mechanistically nonoverlapping with IMinduced apoptosis.