Guidelines for the use and interpretation of assays for monitoring autophagy
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.
Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death
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.
Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes
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.
Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)
There continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes, so it is important to update guidelines for monitoring autophagic activity in different organisms.
The mammalian ultraviolet response is triggered by activation of src tyrosine kinases
Cyclophilin D-dependent mitochondrial permeability transition regulates some necrotic but not apoptotic cell death
Enhancing Macroautophagy Protects against Ischemia/Reperfusion Injury in Cardiac Myocytes*
It is found that autophagic flux is impaired at the level of both induction and degradation and that enhancing autophagy constitutes a powerful and previously uncharacterized protective mechanism against I/R injury to the heart cell.
Response to myocardial ischemia/reperfusion injury involves Bnip3 and autophagy
The results suggest that Bnip3 contributes to I/R injury which triggers a protective stress response with upregulation of autophagy and removal of damaged mitochondria.
Reperfusion injury induces apoptosis in rabbit cardiomyocytes.
- R. Gottlieb, K. Burleson, R. Kloner, B. Babior, R. Engler
- Biology, MedicineJournal of Clinical Investigation
- 1 October 1994
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.
Bid Is Cleaved by Calpain to an Active Fragment in Vitro and during Myocardial Ischemia/Reperfusion*
- M. Chen, H. He, S. Zhan, S. Krajewski, John Calvin Reed, R. Gottlieb
- Biology, MedicineJournal of Biological Chemistry
- 17 August 2001
Findings suggest that there is cross-talk between apoptotic and necrotic pathways in myocardial ischemia/reperfusion injury.