The DOI matches its Crossref record; 137 of the 137 references it cites were found in a registry or an index.
Protein carbonylation, cellular dysfunction, and disease progression
Open accessAbstract
Carbonylation of proteins is an irreversible oxidative damage, often leading to a loss of protein function, which is considered a widespread indicator of severe oxidative damage and disease-derived protein dysfunction. Whereas moderately carbonylated proteins are degraded by the proteasomal system, heavily carbonylated proteins tend to form high-molecular-weight aggregates that are resistant to degradation and accumulate as damaged or unfolded proteins. Such aggregates of carbonylated proteins can inhibit proteasome activity. Alarge number of neurodegenerative diseases are directly associated with the accumulation of proteolysis-resistant aggregates of carbonylated proteins in tissues. Identification of specific carbonylated protein(s) functionally impaired and development of selective carbonyl blockers should lead to the definitive assessment of the causative, correlative or consequential role of protein carbonylation in disease onset and/or progression, possibly providing new therapeutic approaches.
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Cites
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Protein oxidation and peroxidation
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Metadata
- Authors
- Dalle-Donne, I., Aldini, G., Carini, M., Colombo, R., Rossi, R., & Milzani, A.
- Venue
- Journal of Cellular and Molecular Medicine
- Publisher
- Wiley
- Published
- 2006-04
- Volume
- 10
- Issue
- 2
- Pages
- 389-406
- ISSN
- 1582-1838 (ISSN-L)
- OpenAlex
- W2086561195
- Cited by
- 831
- References
- 137
- FWCI
- 11.54
- Type
- journal article
- Language
- en
- Open access
- green
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- Dalle-Donne, I., Aldini, G., Carini, M., Colombo, R., Rossi, R., & Milzani, A. (2006). Protein carbonylation, cellular dysfunction, and disease progression. Journal of Cellular and Molecular Medicine. https://doi.org/10.1111/j.1582-4934.2006.tb00407.x
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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.