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A J McGahon
Researcher at La Jolla Institute for Allergy and Immunology
Publications - 18
Citations - 5983
A J McGahon is an academic researcher from La Jolla Institute for Allergy and Immunology. The author has contributed to research in topics: Apoptosis & Programmed cell death. The author has an hindex of 16, co-authored 18 publications receiving 5879 citations. Previous affiliations of A J McGahon include St Patrick's College, Dublin & University College Cork.
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Journal ArticleDOI
Early redistribution of plasma membrane phosphatidylserine is a general feature of apoptosis regardless of the initiating stimulus: inhibition by overexpression of Bcl-2 and Abl.
Seamus J. Martin,Chris P. M. Reutelingsperger,A J McGahon,J. A. Rader,R. C. A. A. Van Schie,Drake LaFace,Douglas R. Green +6 more
TL;DR: It is shown that PS externalization is an early and widespread event during apoptosis of a variety of murine and human cell types, regardless of the initiating stimulus, and precedes several other events normally associated with this mode of cell death.
Book ChapterDOI
The end of the (cell) line: methods for the study of apoptosis in vitro.
A J McGahon,Seamus J. Martin,Reid P. Bissonnette,Artin Mahboubi,Yufang Shi,Rona J. Mogil,Walter K. Nishioka,Douglas R. Green +7 more
TL;DR: This chapter describes cell death assays that are based on the observation that apoptosis is accompanied by DNA fragmentation, either into the classical “ladder” pattern of 200 bp integer multiples, 50kb fragments, or single-stranded DNA cleavage.
Journal ArticleDOI
Proteolysis of Fodrin (Non-erythroid Spectrin) during Apoptosis
Seamus J. Martin,Geraldine A. O'Brien,Walter K. Nishioka,A J McGahon,Artin Mahboubi,Takaomi C. Saido,Douglas R. Green +6 more
TL;DR: It is demonstrated that cleavage of α-fodrin (non-erythroid spectrin) accompanies apoptosis, induced by activation via the CD3/T cell receptor complex in a murine T cell hybridoma, ligation of the Fas molecule on a human T cell lymphoma line and other Fas-expressing cells, or treatment of cells with staurosporine, dexamethasone, or synthetic ceramide.
Journal ArticleDOI
BCR-ABL Maintains Resistance of Chronic Myelogenous Leukemia Cells to Apoptotic Cell Death
A J McGahon,Reid P. Bissonnette,Reid P. Bissonnette,Manfred Schmitt,Manfred Schmitt,Kate M. Cotter,Kate M. Cotter,Douglas R. Green,Douglas R. Green,Thomas G. Cotter,Thomas G. Cotter +10 more
TL;DR: In this article, the authors showed that BCR-ABL fusion protein acts as an anti-apoptosis gene in CML cells and suggests that the effect is dependent on the abl kinase activity in this chimeric protein.
Journal ArticleDOI
BCR-ABL maintains resistance of chronic myelogenous leukemia cells to apoptotic cell death [published erratum appears in Blood 1994 Jun 15;83(12):3835]
TL;DR: In this paper, the authors show that BCR-ABL fusion protein can be used as an anti-apoptosis gene in CML cells and suggests that the effect is dependent on the abl kinase activity in this chimeric protein.