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Roberta A. Gottlieb

Researcher at Cedars-Sinai Medical Center

Publications -  244
Citations -  35518

Roberta A. Gottlieb is an academic researcher from Cedars-Sinai Medical Center. The author has contributed to research in topics: Autophagy & Mitochondrion. The author has an hindex of 77, co-authored 235 publications receiving 31428 citations. Previous affiliations of Roberta A. Gottlieb include Scripps Health & Scripps Research Institute.

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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

Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes

Daniel J. Klionsky, +235 more
- 16 Feb 2008 - 
TL;DR: A set of guidelines for the selection and interpretation of the methods that can be used by investigators who are attempting to examine macroautophagy and related processes, as well as by reviewers who need to provide realistic and reasonable critiques of papers that investigate these processes are presented.
Journal ArticleDOI

Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death

Christopher P. Baines, +11 more
- 31 Mar 2005 - 
TL;DR: Cyclophilin D and the mitochondrial permeability transition are required for mediating Ca2+- and oxidative damage-induced cell death, but not Bcl-2 family member-regulated death.
Journal ArticleDOI

Reperfusion injury induces apoptosis in rabbit cardiomyocytes.

Roberta A. Gottlieb, +4 more
- 01 Oct 1994 - 
TL;DR: Parts of apoptosis (programmed cell death) in myocytes are identified as a response to reperfusion but not ischemia, which indicates that apoptosis may be a specific feature of reperfusions injury in cardiac myocytes, leading to late cell death.