The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Accumulation of the Authentic Parkin Substrate Aminoacyl-tRNA Synthetase Cofactor, p38/JTV-1, Leads to Catecholaminergic Cell Death
Open accessAbstract
Autosomal-recessive juvenile parkinsonism (AR-JP) is caused by loss-of-function mutations of the parkin gene. Parkin, a RING-type E3 ubiquitin ligase, is responsible for the ubiquitination and degradation of substrate proteins that are important in the survival of dopamine neurons in Parkinson's disease (PD). Accordingly, the abnormal accumulation of neurotoxic parkin substrates attributable to loss of parkin function may be the cause of neurodegeneration in parkin-related parkinsonism. We evaluated the known parkin substrates identified to date in parkin null mice to determine whether the absence of parkin results in accumulation of these substrates. Here we show that only the aminoacyl-tRNA synthetase cofactor p38 is upregulated in the ventral midbrain/hindbrain of both young and old parkin null mice. Consistent with upregulation in parkin knock-out mice, brains of AR-JP and idiopathic PD and diffuse Lewy body disease also exhibit increased level of p38. In addition, p38 interacts with parkin and parkin ubiquitinates and targets p38 for degradation. Furthermore, overexpression of p38 induces cell death that increases with tumor necrosis factor-α treatment and parkin blocks the pro-cell death effect of p38, whereas the R42P, familial-linked mutant of parkin, fails to rescue cell death. We further show that adenovirus-mediated overexpression of p38 in the substantia nigra in mice leads to loss of dopaminergic neurons. Together, our study represents a major advance in our understanding of parkin function, because it clearly identifies p38 as an important authentic pathophysiologic substrate of parkin. Moreover, these results have important implications for understanding the molecular mechanisms of neurodegeneration in PD.
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Cites
Mutation in the α-Synuclein Gene Identified in Families with Parkinson's Disease
Polymeropoulos, M. H., Lavedan, C., Leroy, E., Ide, S. E., Dehejia, A., Dutra, A., Pike, B., Root, H., Rubenstein, J., Boyer, R., et al. (1997) · Science · doi:10.1126/science.276.5321.2045 · Cited by 8,240
Hereditary Early-Onset Parkinson's Disease Caused by Mutations in PINK1
Valente, E. M., Abou-Sleiman, P. M., Caputo, V., Muqit, M. M. K., Harvey, K., Gispert, S., Ali, Z., Del Turco, D., Bentivoglio, A. R., Healy, D. G., et al. (2004) · Science · doi:10.1126/science.1096284 · Cited by 3,481
Familial Parkinson disease gene product, parkin, is a ubiquitin-protein ligase
Shimura, H., Hattori, N., Kubo, S.-I., Mizuno, Y., Asakawa, S., Minoshima, S., Shimizu, N., Iwai, K., Chiba, T., Tanaka, K., et al. (2000) · Nature Genetics · doi:10.1038/77060 · Cited by 2,024 · cited 1×
“The finding that parkin is an ubiquitin E3 ligase provided an important link between protein aggregation and the ubiquitin-proteasome system (UPS) in the pathogenesis of PD (Shimura et al., 2000; Zhang et al., 2000).”
BackgroundShimura, H., Schlossmacher, M. G., Hattori, N., Frosch, M. P., Trockenbacher, A., Schneider, R., Mizuno, Y., Kosik, K. S., & Selkoe, D. J. (2001) · Science · doi:10.1126/science.1060627 · Cited by 1,053
Zhang, Y., Gao, J., Chung, K. K. K., Huang, H., Dawson, V. L., & Dawson, T. M. (2000) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.240347797 · Cited by 982
Self-citationParkin-deficient Mice Exhibit Nigrostriatal Deficits but Not Loss of Dopaminergic Neurons
Goldberg, M. S., Fleming, S. M., Palacino, J. J., Cepeda, C., Lam, H. A., Bhatnagar, A., Meloni, E. G., Wu, N., Ackerson, L. C., Klapstein, G. J., et al. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m308947200 · Cited by 913
Chung, K. K. K., Zhang, Y., Lim, K. L., Tanaka, Y., Huang, H., Gao, J., Ross, C. A., Dawson, V. L., & Dawson, T. M. (2001) · Nature Medicine · doi:10.1038/nm1001-1144 · Cited by 750
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PARIS (ZNF746) Repression of PGC-1α Contributes to Neurodegeneration in Parkinson's Disease
Shin, J.-H., Ko, H. S., Kang, H., Lee, Y., Lee, Y.-I., Pletinkova, O., Troconso, J. C., Dawson, V. L., & Dawson, T. M. (2011) · Cell · doi:10.1016/j.cell.2011.02.010 · Cited by 953
Self-citationExpanding insights of mitochondrial dysfunction in Parkinson's disease
Abou-Sleiman, P. M., Muqit, M. M. K., & Wood, N. W. (2006) · Nature Reviews Neuroscience · doi:10.1038/nrn1868 · Cited by 869
Genetics of Parkinson disease: paradigm shifts and future prospects
Farrer, M. J. (2006) · Nature Reviews Genetics · doi:10.1038/nrg1831 · Cited by 707
Building and decoding ubiquitin chains for mitophagy
Harper, J. W., Ordureau, A., & Heo, J.-M. (2018) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm.2017.129 · Cited by 666
Ge, P., Dawson, V. L., & Dawson, T. M. (2020) · Molecular Neurodegeneration · doi:10.1186/s13024-020-00367-7 · Cited by 496
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Metadata
- Authors
- Ko, H. S., von Coelln, R., Sriram, S. R., Kim, S. W., Chung, K. K. K., Pletnikova, O., Troncoso, J., Johnson, B., Saffary, R., Goh, E. L., Song, H., Park, B.-J., Kim, M. J., Kim, S., Dawson, V. L., & Dawson, T. M.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2005-08-31
- Volume
- 25
- Issue
- 35
- Pages
- 7968-7978
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W2152330309
- Cited by
- 247
- References
- 7
- FWCI
- 15.53
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- CoChat. (2026). Citation check: Accumulation of the Authentic Parkin Substrate Aminoacyl-tRNA Synthetase Cofactor, p38/JTV-1, Leads to Catecholaminergic Cell Death. https://app.cochat.ai/papers/10.1523/jneurosci.2172-05.2005
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- Ko, H. S., von Coelln, R., Sriram, S. R., Kim, S. W., Chung, K. K. K., Pletnikova, O., Troncoso, J., Johnson, B., Saffary, R., Goh, E. L., Song, H., Park, B.-J., Kim, M. J., Kim, S., Dawson, V. L., & Dawson, T. M. (2005). Accumulation of the Authentic Parkin Substrate Aminoacyl-tRNA Synthetase Cofactor, p38/JTV-1, Leads to Catecholaminergic Cell Death. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.2172-05.2005
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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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