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John C. Reed

Researcher at Sanford-Burnham Institute for Medical Research

Publications -  898
Citations -  170817

John C. Reed is an academic researcher from Sanford-Burnham Institute for Medical Research. The author has contributed to research in topics: Apoptosis & Programmed cell death. The author has an hindex of 190, co-authored 891 publications receiving 164382 citations. Previous affiliations of John C. Reed include University of California, San Diego & Discovery Institute.

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Mitochondria and apoptosis

Douglas R. Green, +1 more
- 28 Aug 1998 - 
TL;DR: A variety of key events in apoptosis focus on mitochondria, including the release of caspase activators (such as cytochrome c), changes in electron transport, loss of mitochondrial transmembrane potential, altered cellular oxidation-reduction, and participation of pro- and antiapoptotic Bcl-2 family proteins.
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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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Tumor suppressor p53 is a direct transcriptional activator of the human bax gene

T Miyashita, +1 more
- 27 Jan 1995 - 
TL;DR: The bax gene promoter region contains four motifs with homology to consensus p53-binding sites and wild-type but not mutant p53 protein bound to oligonucleotides corresponding to this region of the bax promoter, suggesting that bax is a p53 primary-response gene, presumably involved in a p 53-regulated pathway for induction of apoptosis.
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Regulation of Cell Death Protease Caspase-9 by Phosphorylation

Michael H. Cardone, +7 more
- 13 Nov 1998 - 
TL;DR: In this paper, the kinase Akt and p21-Ras, an Akt activator, induced phosphorylation of pro-caspase-9 (pro-Casp9) in cells.
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An inhibitor of Bcl-2 family proteins induces regression of solid tumours

Tilman Oltersdorf, +33 more
- 02 Jun 2005 - 
TL;DR: Mechanistic studies reveal that ABT-737 does not directly initiate the apoptotic process, but enhances the effects of death signals, displaying synergistic cytotoxicity with chemotherapeutics and radiation.