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Requirement of JNK for Stress- Induced Activation of the Cytochrome c-Mediated Death Pathway
Cathy Tournier,1
Patricia Hess,1
Derek D. Yang,2*
Jie Xu,2
Tod K. Turner,3
Anjaruwee Nimnual,4
Dafna Bar-Sagi,4
Stephen N. Jones,3
Richard A. Flavell,2
Roger J. Davis1
The c-Jun NH2-terminal kinase (JNK) is activated when
cells are exposed to ultraviolet (UV) radiation. However, the
functionalconsequence of JNK activation in UV-irradiated cells has not
beenestablished. It is shown here that JNK is required for UV-inducedapoptosis in primary murine embryonic fibroblasts. Fibroblastswith
simultaneous targeted disruptions of all the functional Jnkgenes were protected against UV-stimulated apoptosis. The absenceof
JNK caused a defect in the mitochondrial death signaling pathway,including the failure to release cytochrome c. These data indicatethat
mitochondria are influenced by proapoptotic signal transductionthrough
the JNK pathway.
1 Howard Hughes Medical Institute, Program in
Molecular Medicine, Department of Biochemistry & Molecular Biology,
University of Massachusetts Medical School, Worcester, MA 01605, USA.
2 Howard Hughes Medical Institute, Section of
Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.
3 Department of Cell Biology, University of
Massachusetts Medical School, Worcester, MA 01605, USA.
4 Department of Molecular Genetics and Microbiology,
State University of New York at Stony Brook, Stony Brook, NY 11794, USA.
*
Present address: Lilly Research Laboratories, Eli Lilly and
Company, Indianapolis, IN 46285, USA.
To whom correspondence should be addressed. E-mail:
Roger.Davis{at}umassmed.edu
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In Science Signaling
EDITORS' CHOICE
(31 October 2000) Sci. STKE2000 (56), tw9.
[DOI: 10.1126/stke.2000.56.tw9] |Abstract »|Full Text »
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Enhancement of DNA topoisomerase I inhibitor-induced apoptosis by ursodeoxycholic acid.
T. Ikegami, Y. Matsuzaki, M. Al Rashid, S. Ceryak, Y. Zhang, and B. Bouscarel (2006)
Mol. Cancer Ther.
5, 68-79
|Abstract »|Full Text »|PDF »
Genetic deletion of Cdc42GAP reveals a role of Cdc42 in erythropoiesis and hematopoietic stem/progenitor cell survival, adhesion, and engraftment.
L. Wang, L. Yang, M.-D. Filippi, D. A. Williams, and Y. Zheng (2006)
Blood
107, 98-105
|Abstract »|Full Text »|PDF »
The tyrphostin adaphostin interacts synergistically with proteasome inhibitors to induce apoptosis in human leukemia cells through a reactive oxygen species (ROS)-dependent mechanism.
G. Dasmahapatra, M. Rahmani, P. Dent, and S. Grant (2006)
Blood
107, 232-240
|Abstract »|Full Text »|PDF »
Synergistic antileukemic interactions between 2-medroxyestradiol (2-ME) and histone deacetylase inhibitors involve Akt down-regulation and oxidative stress.
N. Gao, M. Rahmani, X. Shi, P. Dent, and S. Grant (2006)
Blood
107, 241-249
|Abstract »|Full Text »|PDF »
PAK4 Functions in Tumor Necrosis Factor (TNF) {alpha}-induced Survival Pathways by Facilitating TRADD Binding to the TNF Receptor.
Bortezomib Sensitizes Pancreatic Cancer Cells to Endoplasmic Reticulum Stress-Mediated Apoptosis.
S. T. Nawrocki, J. S. Carew, M. S. Pino, R. A. Highshaw, K. Dunner Jr., P. Huang, J. L. Abbruzzese, and D. J. McConkey (2005)
Cancer Res.
65, 11658-11666
|Abstract »|Full Text »|PDF »
Parthenolide sensitizes ultraviolet (UV)-B-induced apoptosis via protein kinase C-dependent pathways.
Hsp70 Inhibits Heat-induced Apoptosis Upstream of Mitochondria by Preventing Bax Translocation.
A. R. Stankiewicz, G. Lachapelle, C. P. Z. Foo, S. M. Radicioni, and D. D. Mosser (2005)
J. Biol. Chem.
280, 38729-38739
|Abstract »|Full Text »|PDF »
Genetic Inhibition or Activation of JNK1/2 Protects the Myocardium from Ischemia-Reperfusion-induced Cell Death in Vivo.
R. A. Kaiser, Q. Liang, O. Bueno, Y. Huang, T. Lackey, R. Klevitsky, T. E. Hewett, and J. D. Molkentin (2005)
J. Biol. Chem.
280, 32602-32608
|Abstract »|Full Text »|PDF »
Cdc42GAP regulates c-Jun N-terminal kinase (JNK)-mediated apoptosis and cell number during mammalian perinatal growth.
L. Wang, L. Yang, K. Burns, C.-Y. Kuan, and Y. Zheng (2005)
PNAS
102, 13484-13489
|Abstract »|Full Text »|PDF »
BAD Ser128 Is Not Phosphorylated by c-Jun NH2-Terminal Kinase for Promoting Apoptosis.
Protein phosphatase subunit G5PR is needed for inhibition of B cell receptor-induced apoptosis.
Y. Xing, H. Igarashi, X. Wang, and N. Sakaguchi (2005)
J. Exp. Med.
202, 707-719
|Abstract »|Full Text »|PDF »
Proteinase-Activated Receptor-1 Mediates Elastase-Induced Apoptosis of Human Lung Epithelial Cells.
T. Suzuki, T. J. Moraes, E. Vachon, H. H. Ginzberg, T.-T. Huang, M. A. Matthay, M. D. Hollenberg, J. Marshall, C. A. G. McCulloch, M. T. H. Abreu, et al. (2005)
Am. J. Respir. Cell Mol. Biol.
33, 231-247
|Abstract »|Full Text »|PDF »
