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Orian S. Shirihai

Researcher at University of California, Los Angeles

Publications -  201
Citations -  29478

Orian S. Shirihai is an academic researcher from University of California, Los Angeles. The author has contributed to research in topics: Mitochondrion & mitochondrial fusion. The author has an hindex of 62, co-authored 179 publications receiving 24576 citations. Previous affiliations of Orian S. Shirihai include Tufts University & Ben-Gurion University of the Negev.

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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

Fission and selective fusion govern mitochondrial segregation and elimination by autophagy

Gilad Twig, +17 more
- 23 Jan 2008 - 
TL;DR: Pulse chase and arrest of autophagy at the pre‐proteolysis stage reveal that fission followed by selective fusion segregates dysfunctional mitochondria and permits their removal by autophagic.
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Pancreatic cancers require autophagy for tumor growth

Shenghong Yang, +16 more
- 01 Apr 2011 - 
TL;DR: Inhibition of autophagy by genetic means or chloroquine treatment leads to robust tumor regression and prolonged survival in pancreatic cancer xenografts and genetic mouse models, and drugs that inactivate this process may have a unique clinical utility in treating pancreatic cancers and other malignancies with a similar dependence on Autophagy.
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Telomere dysfunction induces metabolic and mitochondrial compromise

Ergiin Sahin, +29 more
- 17 Feb 2011 - 
TL;DR: It is shown that enforced Tert or PGC-1α expression or germline deletion of p53 substantially restores PGC network expression, mitochondrial respiration, cardiac function and gluconeogenesis in the setting of telomere dysfunction.