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Cited by 340

The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

Signal Transduction Pathways Regulated by Mitogen-activated/Extracellular Response Kinase Kinase Kinase Induce Cell Death

Open access
Johnson, Nancy Lassignal, Gardner, Anne M., Diener, Katrina M., Lange-Carter, Carol A., Gleavy, Janice, Jarpe, Matthew B., Minden, Audrey, Karin, Michael, Zon, Leonard I., Johnson, Gary L.·1996·Journal of Biological Chemistry

Abstract

Mitogen-activated/extracellular response kinase kinase (MEK) kinase (MEKK) is a serine-threonine kinase that regulates sequential protein phosphorylation pathways, leading to the activation of mitogen-activated protein kinases (MAPK), including members of the Jun kinase (JNK)/stress-activated protein kinase (SAPK) family. In Swiss 3T3 and REF52 fibroblasts, activated MEKK induces cell death involving cytoplasmic shrinkage, nuclear condensation, and DNA fragmentation characteristic of apoptosis. Expression of activated MEKK enhanced the apoptotic response to ultraviolet irradiation, indicating that MEKK-regulated pathways sensitize cells to apoptotic stimuli. Inducible expression of activated MEKK stimulated the transactivation of c-Myc and Elk-1. Activated Raf, the serine-threonine protein kinase that activates the ERK members of the MAPK family, stimulated Elk-1 transactivation but not c-Myc; expression of activated Raf does not induce any of the cellular changes associated with MEKK-mediated cell death. Thus, MEKK selectively regulates signal transduction pathways that contribute to the apoptotic response.

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Crossref · 10.1074/jbc.271.6.3229

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Metadata

Authors
Johnson, N. L., Gardner, A. M., Diener, K. M., Lange-Carter, C. A., Gleavy, J., Jarpe, M. B., Minden, A., Karin, M., Zon, L. I., & Johnson, G. L.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
1996-02
Volume
271
Issue
6
Pages
3229-3237
ISSN
0021-9258 (ISSN-L)
OpenAlex
W2062412222
Cited by
340
References
2
FWCI
18.18
Type
journal article
Language
en
Open access
hybrid

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