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Lawrence H. Boise

Researcher at Emory University

Publications -  240
Citations -  32183

Lawrence H. Boise is an academic researcher from Emory University. The author has contributed to research in topics: Apoptosis & Multiple myeloma. The author has an hindex of 62, co-authored 220 publications receiving 28897 citations. Previous affiliations of Lawrence H. Boise include University of Chicago & Virginia Commonwealth University.

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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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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.
Journal ArticleDOI

bcl-x, a bcl-2-related gene that functions as a dominant regulator of apoptotic cell death

Lawrence H. Boise, +8 more
- 27 Aug 1993 - 
TL;DR: Data suggest that bcl-x plays an important role in both positive and negative regulation of programmed cell death, as well as in tissues containing long-lived postmitotic cells, such as adult brain.
Journal ArticleDOI

Bad, a heterodimeric partner for Bcl-xL and Bcl-2, displaces bax and promotes cell death

Elizabeth Yang, +5 more
- 27 Jan 1995 - 
TL;DR: A novel interacting protein, Bad, whose homology to Bcl-2 is limited to the BH1 and BH2 domains is identified, whose role in the mammalian cell death pathway is determined by these competing dimerizations in which levels of Bad influence the effectiveness of BCl-2 versus B cl-xL in repressing death.
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CD28 costimulation can promote T cell survival by enhancing the expression of Bcl-xL

Lawrence H. Boise, +6 more
- 01 Jul 1995 - 
TL;DR: Data demonstrating that CD28 costimulation enhances the in vitro survival of activated T cells and suggesting that an important role of CD28costimulation is to augment T cell survival during antigen activation is suggested.