Requirement of JNK for Stress- Induced Activation of the Cytochrome c-Mediated Death Pathway
Abstract
The c-Jun NH 2 -terminal kinase (JNK) is activated when cells are exposed to ultraviolet (UV) radiation. However, the functional consequence of JNK activation in UV-irradiated cells has not been established. It is shown here that JNK is required for UV-induced apoptosis in primary murine embryonic fibroblasts. Fibroblasts with simultaneous targeted disruptions of all the functional Jnk genes were protected against UV-stimulated apoptosis. The absence of JNK caused a defect in the mitochondrial death signaling pathway, including the failure to release cytochrome c. These data indicate that mitochondria are influenced by proapoptotic signal transduction through the JNK pathway.
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Absence of JNK limits UV stress-induced mitochondrial release of cytochrome c.
“The absence of JNK was previously shown to limit uv stress-induced mitochondrial release of cytochrome c (422),”
From Redox regulation of mitochondrial function (2012) · cites this paper as [422]
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- Authors
- Tournier, C., Hess, P., Yang, D. D., Xu, J., Turner, T. K., Nimnual, A., Bar-Sagi, D., Jones, S. N., Flavell, R. A., & Davis, R. J.
- Affiliations
- Howard Hughes Medical Institute (US)
- University of Massachusetts Chan Medical School (US)
- Stony Brook University (US)
- Department of Molecular Genetics and Microbiology, State University of New York at Stony Brook, Stony Brook, NY 11794, USA.
- Corresponding author
- Yang, Derek D.
- Davis, Roger J.
- Venue
- Science
- Published
- 2000-05-05
- Volume
- 288
- Issue
- 5467
- Pages
- 870-874
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2119807130
- Cited by
- 1,728
- References
- 42
- Citations by year
- 2026: 15 · 2025: 20 · 2024: 15 · 2023: 25 · 2022: 25 · 2021: 46 · 2020: 45 · 2019: 31 · 2018: 37 · 2017: 46 · 2016: 36 · 2015: 41 · 2014: 47 · 2013: 64 · 2012: 69
- FWCI
- 49.56
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Research Explorer (The University of Manchester) (publishedVersion)
- eScholarship@UMassChan (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- JNK, c-Jun NH2-terminal kinase, cytochrome c release, mitochondrial apoptosis, UV-induced apoptosis, stress-induced apoptosis, embryonic fibroblasts
- MeSH terms
- Animals, Cell Count, Cell Division, Cells, Cultured, Cytochrome c Group, Enzyme Activation, Fibroblasts, Methyl Methanesulfonate, Mitochondria, Proteins, Proto-Oncogene Proteins, Ultraviolet Rays, Tumor Suppressor Protein p53, NF-kappa B, Apoptosis, Protein Serine-Threonine Kinases, Gene Targeting, Proto-Oncogene Proteins c-bcl-2, Caspases, Mitogen-Activated Protein Kinases, MAP Kinase Signaling System, JNK Mitogen-Activated Protein Kinases, Proto-Oncogene Proteins c-akt, Mice, Caspase 3, Caspase 9, Apoptotic Protease-Activating Factor 1, DNA Fragmentation
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