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Ben A. Bahr

Researcher at University of Connecticut

Publications -  43
Citations -  10249

Ben A. Bahr is an academic researcher from University of Connecticut. The author has contributed to research in topics: Receptor & Calpain. The author has an hindex of 28, co-authored 41 publications receiving 9218 citations. Previous affiliations of Ben A. Bahr include University of North Carolina at Pembroke & University of Colorado Denver.

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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.
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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.
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Synergistic Activation of Caspase-3 by m-Calpain after Neonatal Hypoxia-Ischemia A MECHANISM OF “PATHOLOGICAL APOPTOSIS”?

Klas Blomgren, +9 more
- 30 Mar 2001 - 
TL;DR: This is the first report to the authors' knowledge suggesting a direct link between the early, excitotoxic, calcium-mediated activation of calpain after cerebral hypoxia-ischemia and the subsequent activation of caspase-3, thus representing a tentative pathway of “pathological apoptosis.”
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The influence of age on apoptotic and other mechanisms of cell death after cerebral hypoxia-ischemia.

Changlian Zhu, +11 more
- 01 Feb 2005 - 
TL;DR: To the authors' knowledge, this is the first report demonstrating developmental regulation of AIF-mediated cell death as well as involvement of autophagy in a model of brain injury.
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The pathogenic activation of calpain: a marker and mediator of cellular toxicity and disease states.

Peter W. Vanderklish, +1 more
- 01 Oct 2000 - 
TL;DR: Sensitive spectrin breakdown assays now are utilized to identify potential toxic side‐effects of compounds and to develop calpain inhibitors for a wide range of indications including stroke, cerebral vasospasm, and kidney failure.