The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Familial-associated mutations differentially disrupt the solubility, localization, binding and ubiquitination properties of parkin
Abstract
Mutations in parkin are largely associated with autosomal recessive juvenile parkinsonism. The underlying mechanism of pathogenesis in parkin-associated Parkinson's disease (PD) is thought to be due to the loss of parkin's E3 ubiquitin ligase activity. A subset of missense and nonsense point mutations in parkin that span the entire gene and represent the numerous inheritance patterns that are associated with parkin-linked PD were investigated for their E3 ligase activity, localization and their ability to bind, ubiquitinate and effect the degradation of two substrates, synphilin-1 and aminoacyl-tRNA synthetase complex cofactor, p38. Parkin mutants vary in their intracellular localization, binding to substrates and enzymatic activity, yet they are ultimately deficient in their ability to degrade substrate. These results suggest that not all parkin mutations result in loss of parkin's E3 ligase activity, but they all appear to manifest as loss-of-function mutants due to defects in solubility, aggregation, enzymatic activity or targeting proteins to the proteasome for degradation.
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Cites
Aggresomes: A Cellular Response to Misfolded Proteins
Johnston, J. A., Ward, C. L., & Kopito, R. R. (1998) · The Journal of Cell Biology · doi:10.1083/jcb.143.7.1883 · Cited by 2,148
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 2×
“Parkin self-ubiquitination has been established as a reliable method to study parkin’s enzymatic function as parkin is capable of auto-ubiquitination (18,25,37).”
BackgroundMethodMitochondrial pathology and apoptotic muscle degeneration in Drosophila parkin mutants
Greene, J. C., Whitworth, A. J., Kuo, I., Andrews, L. A., Feany, M. B., & Pallanck, L. J. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0737556100 · Cited by 1,203
Shimura, 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
Self-citationParkin-deficient mice are not a robust model of parkinsonism
Perez, F. A., & Palmiter, R. D. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0409598102 · Cited by 477
Cited by
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-citationWong, Y. C., & Holzbaur, E. L. F. (2014) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1405752111 · Cited by 812
Genetics of Parkinson disease: paradigm shifts and future prospects
Farrer, M. J. (2006) · Nature Reviews Genetics · doi:10.1038/nrg1831 · Cited by 707
Mitochondrial dysfunction in Parkinson's disease
Winklhofer, K. F., & Haass, C. (2010) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2009.08.013 · Cited by 688
Veeriah, S., Taylor, B. S., Meng, S., Fang, F., Yilmaz, E., Vivanco, I., Janakiraman, M., Schultz, N., Hanrahan, A. J., Pao, W., et al. (2010) · Nature Genetics · doi:10.1038/ng.491 · Cited by 406
Metadata
- Authors
- Sriram, S. R., Li, X., Ko, H. S., Chung, K. K. K., Wong, E., Lim, K. L., Dawson, V. L., & Dawson, T. M.
- Venue
- Human Molecular Genetics
- Publisher
- Oxford University Press (OUP)
- Published
- 2005-07-27
- Volume
- 14
- Issue
- 17
- Pages
- 2571-2586
- ISSN
- 0964-6906 (ISSN-L)
- 1460-2083
- OpenAlex
- W2111542278
- Cited by
- 223
- References
- 8
- FWCI
- 11.09
- Type
- journal article
- Language
- en
- Open access
- closed
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- Sriram, S. R., Li, X., Ko, H. S., Chung, K. K. K., Wong, E., Lim, K. L., Dawson, V. L., & Dawson, T. M. (2005). Familial-associated mutations differentially disrupt the solubility, localization, binding and ubiquitination properties of parkin. Human Molecular Genetics. https://doi.org/10.1093/hmg/ddi292
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