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A c-jun dominant negative mutant protects sympathetic neurons against programmed cell death
Open accessAbstract
Sympathetic neurons depend on nerve growth factor (NGF) for survival and die by apoptosis in its absence. We have investigated the pattern of expression of the Jun and Fos family of transcription factors in dying sympathetic neurons using antibodies specific for each family member. When sympathetic neurons are deprived of NGF, the level of c-Jun protein significantly increases, whereas the levels of the other members of the Jun and Fos family remain relatively constant. c-Jun also becomes more phosphorylated, probably on its amino terminal transactivation domain. When microinjected into sympathetic neurons, an expression vector for a c-Jun dominant negative mutant protects them against NGF withdrawal-induced death, indicating that AP-1 activity is essential for neuronal cell death. Furthermore, overexpression of the full-length c-Jun protein is, in itself, sufficient to induce apoptosis in sympathetic neurons.
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The jun proto-oncogene is positively autoregulated by its product, Jun/AP-1
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Cited by
Ischemic Cell Death in Brain Neurons
Lipton, P. (1999) · Physiological Reviews · doi:10.1152/physrev.1999.79.4.1431 · Cited by 3,043
AP-1 as a regulator of cell life and death
Shaulian, E., & Karin, M. (2002) · Nature Cell Biology · doi:10.1038/ncb0502-e131 · Cited by 2,961
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Diverse functions of JNK signaling and c-Jun in stress response and apoptosis
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Metadata
- Authors
- Ham, J., Babij, C., Whitfield, J., Pfarr, C. M., Lallemand, D., Yaniv, M., & Rubin, L. L.
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 1995-05
- Volume
- 14
- Issue
- 5
- Pages
- 927-939
- ISSN
- 0896-6273 (ISSN-L)
- OpenAlex
- W1968015127
- Cited by
- 796
- References
- 6
- FWCI
- 26.05
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Ham, J., Babij, C., Whitfield, J., Pfarr, C. M., Lallemand, D., Yaniv, M., & Rubin, L. L. (1995). A c-jun dominant negative mutant protects sympathetic neurons against programmed cell death. Neuron. https://doi.org/10.1016/0896-6273(95)90331-3
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