The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Transcriptional repression of p53 by parkin and impairment by mutations associated with autosomal recessive juvenile Parkinson's disease
Open accessAbstract
Mutations of the ubiquitin ligase parkin account for most autosomal recessive forms of juvenile Parkinson's disease (AR-JP). Several studies have suggested that parkin possesses DNA-binding and transcriptional activity. We report here that parkin is a p53 transcriptional repressor. First, parkin prevented 6-hydroxydopamine-induced caspase-3 activation in a p53-dependent manner. Concomitantly, parkin reduced p53 expression and activity, an effect abrogated by familial parkin mutations known to either abolish or preserve its ligase activity. ChIP experiments indicate that overexpressed and endogenous parkin interact physically with the p53 promoter and that pathogenic mutations abolish DNA binding to and promoter transactivation of p53. Parkin lowered p53 mRNA levels and repressed p53 promoter transactivation through its Ring1 domain. Conversely, parkin depletion enhanced p53 expression and mRNA levels in fibroblasts and mouse brains, and increased cellular p53 activity and promoter transactivation in cells. Finally, familial parkin missense and deletion mutations enhanced p53 expression in human brains affected by AR-JP. This study reveals a ubiquitin ligase-independent function of parkin in the control of transcription and a functional link between parkin and p53 that is altered by AR-JP mutations.
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“Parkin can transcriptionally repress p53. Specifically, parkin suppresses p53 promoter transactivation and reduces p53 mRNA levels through its Ring1 domain.240”
From p53: from understanding its structure to advances in therapeutic targeting (2026) · cites this paper as [240]
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Cites
Mdm2 promotes the rapid degradation of p53
Haupt, Y., Maya, R., Kazaz, A., & Oren, M. (1997) · Nature · doi:10.1038/387296a0 · Cited by 4,506
Cellular survival: a play in three Akts
Datta, S. R., Brunet, A., & Greenberg, M. E. (1999) · Genes & Development · doi:10.1101/gad.13.22.2905 · Cited by 4,216
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
Tumor Suppression at the Mouse INK4a Locus Mediated by the Alternative Reading Frame Product p19
Kamijo, T., Zindy, F., Roussel, M. F., Quelle, D. E., Downing, J. R., Ashmun, R. A., Grosveld, G., & Sherr, C. J. (1997) · Cell · doi:10.1016/s0092-8674(00)80452-3 · Cited by 1,566
Parkin-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
Self-citationChung, 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
Parkin protects human dopaminergic neuroblastoma cells against dopamine-induced apoptosis
Jiang, H., Ren, Y., Zhao, J., & Feng, J. (2004) · Human Molecular Genetics · doi:10.1093/hmg/ddh180 · Cited by 239 · cited 1×
“Parkin is associated with auto‑ somal recessive juvenile forms of Parkinson’s disease 1 and has been characterized as a ubiquitin ligase 2 that acts as a negative modulator of apoptosis, both in vitro and in vivo 3,4 .”
Presenilin-Dependent -Secretase-Mediated Control of p53-Associated Cell Death in Alzheimer's Disease
Alves da Costa, C., Sunyach, C., Pardossi-Piquard, R., Sevalle, J., Vincent, B., Boyer, N., Kawarai, T., Girardot, N., St. George-Hyslop, P., & Checler, F. (2006) · Journal of Neuroscience · doi:10.1523/jneurosci.0651-06.2006 · Cited by 168
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Cited by
Kamath, T., Abdulraouf, A., Burris, S. J., Langlieb, J., Gazestani, V., Nadaf, N. M., Balderrama, K., Vanderburg, C., & Macosko, E. Z. (2022) · Nature Neuroscience · doi:10.1038/s41593-022-01061-1 · Cited by 552
Hoshino, A., Mita, Y., Okawa, Y., Ariyoshi, M., Iwai-Kanai, E., Ueyama, T., Ikeda, K., Ogata, T., & Matoba, S. (2013) · Nature Communications · doi:10.1038/ncomms3308 · Cited by 536
Parkin, a p53 target gene, mediates the role of p53 in glucose metabolism and the Warburg effect
Zhang, C., Lin, M., Wu, R., Wang, X., Yang, B., Levine, A. J., Hu, W., & Feng, Z. (2011) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1113884108 · Cited by 431
Implications of glial nitric oxide in neurodegenerative diseases
Yuste, J. E., Tarragon, E., Campuzano, C. M., & Ros-Bernal, F. (2015) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2015.00322 · Cited by 356
Aberrant Protein S-Nitrosylation in Neurodegenerative Diseases
Nakamura, T., Tu, S., Akhtar, M. W., Sunico, C. R., Okamoto, S.-I., & Lipton, S. A. (2013) · Neuron · doi:10.1016/j.neuron.2013.05.005 · Cited by 355
Metadata
- Authors
- da Costa, C. A., Sunyach, C., Giaime, E., West, A., Corti, O., Brice, A., Safe, S., Abou-Sleiman, P. M., Wood, N. W., Takahashi, H., Goldberg, M. S., Shen, J., & Checler, F.
- Venue
- Nature Cell Biology
- Published
- 2009-10-04
- Volume
- 11
- Issue
- 11
- Pages
- 1370-1375
- ISSN
- 1465-7392 (ISSN-L)
- 1476-4679
- OpenAlex
- W1990048226
- Cited by
- 212
- References
- 8
- FWCI
- 9.19
- Type
- journal article
- Language
- en
- Open access
- green
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