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Valentina Sica

Researcher at University of Paris

Publications -  45
Citations -  7506

Valentina Sica is an academic researcher from University of Paris. The author has contributed to research in topics: Autophagy & Mitochondrion. The author has an hindex of 18, co-authored 40 publications receiving 6420 citations. Previous affiliations of Valentina Sica include Paris Descartes University & Pierre-and-Marie-Curie University.

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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.
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Caloric Restriction Mimetics Enhance Anticancer Immunosurveillance

Federico Pietrocola, +35 more
- 11 Jul 2016 - 
TL;DR: Short-term fasting or treatment with several chemically unrelated autophagy-inducing CRMs, including hydroxycitrate and spermidine, improved the inhibition of tumor growth by chemotherapy in vivo and improved anticancer immunosurveillance and reducing tumor mass.
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Spermidine induces autophagy by inhibiting the acetyltransferase EP300.

Federico Pietrocola, +10 more
- 01 Mar 2015 - 
TL;DR: Results support the idea that EP300 acts as an endogenous repressor of autophagy and that potent Autophagy inducers including spermidine de facto act as EP300 inhibitors.
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Crizotinib-induced immunogenic cell death in non-small cell lung cancer

Peng Liu, +34 more
- 02 Apr 2019 - 
TL;DR: It is shown that crizotinib is an effective stimulator of immunogenic cell death and can potentiate the efficacy of immune checkpoint blockade and can exert their anticancer effect through indirect immune-dependent mechanism.
Journal ArticleDOI

Organelle-Specific Initiation of Autophagy

Valentina Sica, +5 more
- 20 Aug 2015 - 
TL;DR: The molecular systems through which specific subcellular compartments-including the nucleus, mitochondria, plasma membrane, reticular apparatus, and cytosol-convert homeostatic perturbations into an increased offer of autophagic substrates or an accrued cellular demand for autophile products or functions are summarized.