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

Xia, Zhengui, Dickens, Martin, Raingeaud, Joël, Davis, Roger J., Greenberg, Michael E.·1995·Science
DOI 10.1126/science.270.5240.1326
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Abstract

Apoptosis plays an important role during neuronal development, and defects in apoptosis may underlie various neurodegenerative disorders. To characterize molecular mechanisms that regulate neuronal apoptosis, the contributions to cell death of mitogen-activated protein (MAP) kinase family members, including ERK (extracellular signal-regulated kinase), JNK (c-JUN NH 2 -terminal protein kinase), and p38, were examined after withdrawal of nerve growth factor (NGF) from rat PC-12 pheochromocytoma cells. NGF withdrawal led to sustained activation of the JNK and p38 enzymes and inhibition of ERKs. 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. Therefore, the dynamic balance between growth factor-activated ERK and stress-activated JNK-p38 pathways may be important in determining whether a cell survives or undergoes apoptosis.

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Items 101–130 of 130

Metadata

Authors
Xia, Z., Dickens, M., Raingeaud, J., Davis, R. J., & Greenberg, M. E.
Venue
Science
Publisher
American Association for the Advancement of Science (AAAS)
Published
1995-11-24
Volume
270
Issue
5240
Pages
1326-1331
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
DOI
10.1126/science.270.5240.1326
OpenAlex
W1976385326
Cited by
5,287
References
6
FWCI
79.93
Type
journal article
Language
en
Open access
closed

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