scispace - formally typeset
D

Dale E. Bredesen

Researcher at University of California, Los Angeles

Publications -  314
Citations -  41668

Dale E. Bredesen is an academic researcher from University of California, Los Angeles. The author has contributed to research in topics: Programmed cell death & Apoptosis. The author has an hindex of 92, co-authored 310 publications receiving 40064 citations. Previous affiliations of Dale E. Bredesen include Sanford-Burnham Institute for Medical Research & University of California, San Diego.

Papers
More filters
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

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

Lorenzo Galluzzi, +103 more
TL;DR: A nonexhaustive comparison of methods to detect cell death with apoptotic or nonapoptotic morphologies, their advantages and pitfalls is provided and the importance of performing multiple, methodologically unrelated assays to quantify dying and dead cells is emphasized.
Journal ArticleDOI

Bcl-2 inhibition of neural death : decreased generation of reactive oxygen species

TL;DR: The proto-oncogene bcl-2 inhibits apoptotic and necrotic neural cell death by decreasing the net cellular generation of reactive oxygen species and lipid peroxides as discussed by the authors.
Journal ArticleDOI

Bax directly induces release of cytochrome c from isolated mitochondria

TL;DR: It is shown that addition of submicromolar amounts of recombinant Bax protein to isolated mitochondria can induce cytochrome c (Cyt c) release, whereas a peptide representing the Bax BH3 domain was inactive, implying that Bax uses an alternative mechanism for triggering release of Cyt c from mitochondria.
Journal ArticleDOI

Coupling endoplasmic reticulum stress to the cell death program.

TL;DR: It is hoped that dissection of the molecular components and pathways that alter ER structure and function and ultimately promote cellular death will provide a framework for understanding degenerative disorders that feature misfolded proteins.