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Steven Grant

Researcher at Virginia Commonwealth University

Publications -  396
Citations -  24309

Steven Grant is an academic researcher from Virginia Commonwealth University. The author has contributed to research in topics: Apoptosis & Kinase. The author has an hindex of 71, co-authored 370 publications receiving 22814 citations. Previous affiliations of Steven Grant include University of Helsinki & VCU Medical Center.

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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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MAPK pathways in radiation responses.

TL;DR: The ability of radiation to activate MAPK signaling pathways may depend on the expression of multiple growth factor receptors, autocrine factors and Ras mutation, and enhanced basal signaling by proto-oncogenes such as K-/H-/N-RAS may provide a radioprotective and growth-promoting signal.
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Stress and radiation-induced activation of multiple intracellular signaling pathways.

TL;DR: This review will attempt to describe some of the complex network of signals induced by ionizing radiation and other cellular stresses in animal cells, with particular attention to signaling by growth factor and death receptors.
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Induction of apoptotic DNA damage and cell death by activation of the sphingomyelin pathway.

TL;DR: Results demonstrate that the ceramicamide-dependent signaling system selectively induces apoptosis and raise the possibility that ceramide-activated enzymes represent important components in a signaling cascade involved in the regulation of programmed cell death.
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Mcl-1 down-regulation potentiates ABT-737 lethality by cooperatively inducing Bak activation and Bax translocation.

TL;DR: These findings suggest down-regulation of Mcl-1 by either CDK inhibitors or genetic approaches dramatically potentiate ABT-737 lethality through cooperative interactions at two distinct levels: unleashing of Bak from both Bcl-xL and M cl-1 and simultaneous induction of Bak activation and Bax translocation.