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Anastasis Stephanou

Researcher at University College London

Publications -  114
Citations -  11146

Anastasis Stephanou is an academic researcher from University College London. The author has contributed to research in topics: Urocortin & Apoptosis. The author has an hindex of 48, co-authored 107 publications receiving 9924 citations. Previous affiliations of Anastasis Stephanou include UCL Institute of Child Health & University of Verona.

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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.
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Apoptosis of Endothelial Cells Precedes Myocyte Cell Apoptosis in Ischemia/Reperfusion Injury

TL;DR: The radial spread of apoptosis to surrounding cardiac myocytes suggests that reperfusion induces the release of soluble pro-apoptotic mediators from endothelial cells that promote myocyte apoptosis.
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Urocortin inhibits Beclin1-mediated autophagic cell death in cardiac myocytes exposed to ischaemia/reperfusion injury

TL;DR: It is demonstrated that autophagy is also induced by a single cycle of ischaemia/reperfusion (I/R in neonatal and adult rat cardiac myocytes) and reduction of Beclin1 expression in cardiac myocyte by RNAi reduces I/R-induced autophileagy and this is associated with enhanced cell survival.
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Urocortin protects against ischemic and reperfusion injury via a MAPK-dependent pathway.

TL;DR: It is reported that UCN prevented cell death when administered to primary cardiac myocyte cultures both prior to simulated hypoxia/ischemia and at the point of reoxygenation after simulated hyp oxia/ISChemia, suggesting a novel function of UCN as a cardioprotective agent that could act when given after ischemia, at reperfusion.
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STAT-1 Interacts with p53 to Enhance DNA Damage-induced Apoptosis

TL;DR: It is shown that STAT-1 is required for optimal DNA damage-induced apoptosis, and is another member of a growing family of protein partners able to modulate the p53-activated apoptotic pathway.