The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Activated c-Jun N-Terminal Kinase Is Required for Axon Formation
Open accessAbstract
A critical transition in neuron development is formation of the axon, which establishes the polarized structure of the neuron that underlies its entire input and output capabilities. The morphological events that occur during axonogenesis have long been known, yet the molecular determinants underlying axonogenesis remain poorly understood. We demonstrate here that axonogenesis requires activated c-Jun N-terminal kinase (JNK). JNK is expressed throughout the neuron, but its phosphorylated, activated form is highly enriched in the axon. In young axons, activated JNK forms a proximodistal gradient of increasing intensity, beginning at about the point where the axon exceeds the lengths of the other neurites (minor processes). Treatment with SP600125, a specific inhibitor of JNK, reversibly inhibits axonogenesis but does not prevent the formation of minor processes or their differentiation into dendrites (based on their immunostaining with marker proteins). Expression of a dominant-negative construct against JNK similarly prevents axonogenesis. Investigation of JNK targets revealed that activating transcription factor-2 is phosphorylated under normal conditions in neurons, and its phosphorylation is significantly attenuated after JNK inhibition. These results demonstrate that activated JNK is required for axonogenesis but not formation of minor processes or development of dendrites.
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Shaner, N. C., Campbell, R. E., Steinbach, P. A., Giepmans, B. N. G., Palmer, A. E., & Tsien, R. Y. (2004) · Nature Biotechnology · doi:10.1038/nbt1037 · Cited by 4,619
SP600125, an anthrapyrazolone inhibitor of Jun N-terminal kinase
Bennett, B. L., Sasaki, D. T., Murray, B. W., O'Leary, E. C., Sakata, S. T., Xu, W., Leisten, J. C., Motiwala, A., Pierce, S., Satoh, Y., et al. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.251194298 · Cited by 2,558 · cited 3×
“…the ATP-binding site in JNK, and appears not to block phosphorylation of JNK by its upstream activating kinases, these results imply that JNK undergoes positive-feedback activation or autophosphorylation within the axon, similar to previous observations in other cell types (Bennett et al., 2001).”
BackgroundResultThe establishment of polarity by hippocampal neurons in culture.
Dotti, C., Sullivan, C., & Banker, G. (1988) · The Journal of Neuroscience · doi:10.1523/jneurosci.08-04-01454.1988 · Cited by 1,862
Self-citationA Cytoplasmic Inhibitor of the JNK Signal Transduction Pathway
Dickens, M., Rogers, J. S., Cavanagh, J., Raitano, A., Xia, Z., Halpern, J. R., Greenberg, M. E., Sawyers, C. L., & Davis, R. J. (1997) · Science · doi:10.1126/science.277.5326.693 · Cited by 675
A Mammalian Scaffold Complex That Selectively Mediates MAP Kinase Activation
Whitmarsh, A. J., Cavanagh, J., Tournier, C., Yasuda, J., & Davis, R. J. (1998) · Science · doi:10.1126/science.281.5383.1671 · Cited by 652 · cited 1×
“Dominant-negative inhibition of JNK prevents axonogenesis To verify our pharmacological results, we used a dominant-negative approach to inhibit JNK. JIP-1 is a scaffolding protein that brings together JNK and its upstream activators (Whitmarsh et al., 1998).”
BackgroundHippocampal Neuronal Polarity Specified by Spatially Localized mPar3/mPar6 and PI 3-Kinase Activity
Shi, S.-H., Jan, L. Y., & Jan, Y.-N. (2003) · Cell · doi:10.1016/s0092-8674(02)01249-7 · Cited by 600
The sequential activity of the GTPases Rap1B and Cdc42 determines neuronal polarity.
Schwamborn, J. C., & Püschel, A. W. (2004) · Nature Neuroscience · doi:10.1038/nn1295 · Cited by 385
Zheng, C., Xiang, J., Hunter, T., & Lin, A. (1999) · Journal of Biological Chemistry · doi:10.1074/jbc.274.41.28966 · Cited by 110
Cited by
Microtubule stabilization specifies initial neuronal polarization
Witte, H., Neukirchen, D., & Bradke, F. (2008) · The Journal of Cell Biology · doi:10.1083/jcb.200707042 · Cited by 564
Establishment of axon-dendrite polarity in developing neurons.
Barnes, A. P., & Polleux, F. (2009) · Annual Review of Neuroscience · doi:10.1146/annurev.neuro.31.060407.125536 · Cited by 523
Fröhlich, D., Kuo, W. P., Frühbeis, C., Sun, J.-J., Zehendner, C. M., Luhmann, H. J., Pinto, S., Toedling, J., Trotter, J., & Krämer-Albers, E.-M. (2014) · Philosophical Transactions of the Royal Society B: Biological Sciences · doi:10.1098/rstb.2013.0510 · Cited by 313
Bernardino, L., Agasse, F., Silva, B., Ferreira, R., Grade, S., & Malva, J. O. (2008) · Stem Cells · doi:10.1634/stemcells.2007-0914 · Cited by 220
MicroRNA-124 loaded nanoparticles enhance brain repair in Parkinson's disease
Saraiva, C., Paiva, J., Santos, T., Ferreira, L., & Bernardino, L. (2016) · Journal of Controlled Release · doi:10.1016/j.jconrel.2016.06.005 · Cited by 169
Metadata
- Authors
- Oliva, A. A., Atkins, C. M., Copenagle, L., & Banker, G. A.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2006-09-13
- Volume
- 26
- Issue
- 37
- Pages
- 9462-9470
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W1973363462
- Cited by
- 158
- References
- 8
- FWCI
- 3.82
- Type
- journal article
- Language
- en
- Open access
- hybrid
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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