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Howard O. Fearnhead

Researcher at National University of Ireland, Galway

Publications -  57
Citations -  8246

Howard O. Fearnhead is an academic researcher from National University of Ireland, Galway. The author has contributed to research in topics: Apoptosis & Programmed cell death. The author has an hindex of 28, co-authored 55 publications receiving 7593 citations. Previous affiliations of Howard O. Fearnhead include National University of Ireland & University of Leicester.

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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.
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Multiple species of cpp32 and mch2 are the major active caspases present in apoptotic cells

TL;DR: It is found that CPP32 ( caspase 3) and Mch2 (caspase 6) are the major active caspases in apoptotic cells, and are activated in response to distinct apoptosis‐inducing stimuli and in all cell lines analyzed.
Journal Article

Formation of large molecular weight fragments of DNA is a key committed step of apoptosis in thymocytes.

TL;DR: It is proposed that the formation of large fragments of DNA represents a key committed step in apoptosis, and that it is from these fragments that the archetypal DNA ladders associated with apoptosis are derived.
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Increased membrane permeability of apoptotic thymocytes: A flow cytometric study

TL;DR: It is shown that the efflux of fluorescein from apoptotic cells is more rapid than that from normal thymocytes, and an increase in the permeability of the plasma membrane of the apoptoticThymocytes results in the more rapid uptake of Hoechst 33342.
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Oncogene-dependent apoptosis is mediated by caspase-9

TL;DR: As predicted by the in vitro system, preventing caspase-9 activation blocked drug-induced apoptosis in cells sensitized by E1A, an adenoviral oncogene.