The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Proteomic analysis of parkin knockout mice: alterations in energy metabolism, protein handling and synaptic function
Open accessAbstract
Parkin knockout (KO) mice show behavioural and biochemical changes that reproduce some of the presymptomatic aspects of Parkinson's disease, in the absence of neuronal degeneration. To provide insight into the pathogenic mechanisms underlying the preclinical stages of parkin‐related parkinsonism, we searched for possible changes in the brain proteome of parkin KO mice by means of fluorescence two‐dimensional difference gel electrophoresis and mass spectrometry. We identified 87 proteins that differed in abundance between wild‐type and parkin KO mice by at least 45%. A high proportion of these proteins were related to energy metabolism. The levels of several proteins involved in detoxification, stress‐related chaperones and components of the ubiquitin–proteasome pathway were also altered. These differences might reflect adaptive mechanisms aimed at compensating for the presence of reactive oxygen species and the accumulation of damaged proteins in parkin KO mice. Furthermore, the up‐regulation of several members of the membrane‐associated guanylate kinase family of synaptic scaffold proteins and several septins, including the Parkin substrate cell division control related protein 1 (CDCRel‐1), may contribute to the abnormalities in neurotransmitter release previously observed in parkin KO mice. This study provides clues into possible compensatory mechanisms that protect dopaminergic neurones from death in parkin KO mice and may help us understand the preclinical deficits observed in parkin‐related parkinsonism.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
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 2×
“Parkin, a 465-amino acid protein with a ubiquitin-like domain at its N-terminus and a C-terminal cysteine-rich RING-IBR-RING motif, has E3 ubiquitin–protein ligase activity that promotes the ubiquitylation and proteasomal degradation of specific protein substrates (Imai et al. 2000; Shimura et al. 2000; Zhang et al. 2…”
BackgroundZhang, 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
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
Castegna, A., Aksenov, M., Aksenova, M., Thongboonkerd, V., Klein, J. B., Pierce, W. M., Booze, R., Markesbery, W. R., & Butterfield, D. A. (2002) · Free Radical Biology and Medicine · doi:10.1016/s0891-5849(02)00914-0 · Cited by 581
Choi, J., Levey, A. I., Weintraub, S. T., Rees, H. D., Gearing, M., Chin, L.-S., & Li, L. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m314124200 · Cited by 568
Parkin-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
The Roles of PINK1, Parkin, and Mitochondrial Fidelity in Parkinson’s Disease
Pickrell, A. M., & Youle, R. J. (2015) · Neuron · doi:10.1016/j.neuron.2014.12.007 · Cited by 2,310
Mitochondrial dysfunction and oxidative stress in Parkinson's disease
Subramaniam, S. R., & Chesselet, M.-F. (2013) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2013.04.004 · Cited by 913
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
Mitochondrial dysfunction in Parkinson’s disease – a key disease hallmark with therapeutic potential
Henrich, M. T., Oertel, W. H., Surmeier, D. J., & Geibl, F. F. (2023) · Molecular Neurodegeneration · doi:10.1186/s13024-023-00676-7 · Cited by 406
Olzmann, J. A., Li, L., Chudaev, M. V., Chen, J., Perez, F. A., Palmiter, R. D., & Chin, L.-S. (2007) · The Journal of Cell Biology · doi:10.1083/jcb.200611128 · Cited by 339
Metadata
- Authors
- Periquet, M., Corti, O., Jacquier, S., & Brice, A.
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2005-09-07
- Volume
- 95
- Issue
- 5
- Pages
- 1259-1276
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W2154506764
- Cited by
- 160
- References
- 7
- FWCI
- 8.67
- Type
- journal article
- Language
- en
- Open access
- bronze
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Proteomic analysis of parkin knockout mice: alterations in energy metabolism, protein handling and synaptic function. https://app.cochat.ai/papers/10.1111/j.1471-4159.2005.03442.x
- The paper
- Periquet, M., Corti, O., Jacquier, S., & Brice, A. (2005). Proteomic analysis of parkin knockout mice: alterations in energy metabolism, protein handling and synaptic function. Journal of Neurochemistry. https://doi.org/10.1111/j.1471-4159.2005.03442.x
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
