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Roger J. Davis

Researcher at University of Massachusetts Medical School

Publications -  508
Citations -  109079

Roger J. Davis is an academic researcher from University of Massachusetts Medical School. The author has contributed to research in topics: Signal transduction & Kinase. The author has an hindex of 147, co-authored 498 publications receiving 103478 citations. Previous affiliations of Roger J. Davis include University of Massachusetts Amherst & University of California, Los Angeles.

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Journal ArticleDOI

Opposing Effects of ERK and JNK-p38 MAP Kinases on Apoptosis

Zhengui Xia, +4 more
- 24 Nov 1995 - 
TL;DR: The effects of dominant-interfering or constitutively activated forms of various components of the JNK-p38 and ERK signaling pathways demonstrated that activation of JNK and p38 and concurrent inhibition of ERK are critical for induction of apoptosis in these cells.
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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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Signal transduction by the JNK group of MAP kinases.

Roger J. Davis
- 13 Oct 2000 - 
TL;DR: This review will focus on the JNK group of MAP kinases, which are characterized by the sequence TEY and the two stress-activatedMAP kinases: p38 with the sequence TGY, and the c-Jun NH2-terminal kinases (JNK) with the sequences TPY.
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JNK1: A protein kinase stimulated by UV light and Ha-Ras that binds and phosphorylates the c-Jun activation domain

Benoit Dérijard, +10 more
- 25 Mar 1994 - 
TL;DR: JNK1 is a component of a novel signal transduction pathway that is activated by oncoproteins and UV irradiation and its properties indicate that JNK1 activation may play an important role in tumor promotion.
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Pro-inflammatory Cytokines and Environmental Stress Cause p38 Mitogen-activated Protein Kinase Activation by Dual Phosphorylation on Tyrosine and Threonine (∗)

Joel Raingeaud, +7 more
- 31 Mar 1995 - 
TL;DR: It is demonstrated that p38, like JNK, is activated by treatment of cells with pro-inflammatory cytokines and environmental stress and the mechanism of p38 activation is mediated by dual phosphorylation on Thr-180 and Tyr-182.