The DOI matches its Crossref record; 209 of the 212 references it cites were found in a registry or an index.
The Roles of PINK1, Parkin, and Mitochondrial Fidelity in Parkinson’s Disease
Open accessAbstract
Understanding the function of genes mutated in hereditary forms of Parkinson's disease yields insight into disease etiology and reveals new pathways in cell biology. Although mutations or variants in many genes increase the susceptibility to Parkinson's disease, only a handful of monogenic causes of parkinsonism have been identified. Biochemical and genetic studies reveal that the products of two genes that are mutated in autosomal recessive parkinsonism, PINK1 and Parkin, normally work together in the same pathway to govern mitochondrial quality control, bolstering previous evidence that mitochondrial damage is involved in Parkinson's disease. PINK1 accumulates on the outer membrane of damaged mitochondria, activates Parkin's E3 ubiquitin ligase activity, and recruits Parkin to the dysfunctional mitochondrion. Then, Parkin ubiquitinates outer mitochondrial membrane proteins to trigger selective autophagy. This review covers the normal functions that PINK1 and Parkin play within cells, their molecular mechanisms of action, and the pathophysiological consequences of their loss.
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“PINK1 plays critical roles in mitochondrial quality control, particularly in induction of mitophagy [39].”
From miR-27a and miR-27b regulate autophagic clearance of damaged mitochondria by targeting PTEN-induced putative kinase 1 (PINK1) (2016) · cites this paper as [39]
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“In PD or AD, only a minor subset of patients has a genetic mutation responsible for disease development (e.g., SNCA , PINK1 and PARK2 mutations in PD (Abeliovich and Gitler, 2016)(Pickrell and Youle, 2015), and APP, PSEN1, PSEN2 in AD (Van Cauwenberghe et al., 2016)).”
From TET2 Regulates the Neuroinflammatory Response in Microglia (2019) · cites this paper as Pickrell and Youle, 2015
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Sequence and organization of the human mitochondrial genome
Anderson, S., Bankier, A. T., Barrell, B. G., de Bruijn, M. H. L., Coulson, A. R., Drouin, J., Eperon, I. C., Nierlich, D. P., Roe, B. A., Sanger, F., et al. (1981) · Nature · doi:10.1038/290457a0 · Cited by 9,740
Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism
Kitada, T., Asakawa, S., Hattori, N., Matsumine, H., Yamamura, Y., Minoshima, S., Yokochi, M., Mizuno, Y., & Shimizu, N. (1998) · Nature · doi:10.1038/33416 · Cited by 5,227
Chronic Parkinsonism in Humans Due to a Product of Meperidine-Analog Synthesis
Langston, J. W., Ballard, P., Tetrud, J. W., & Irwin, I. (1983) · Science · doi:10.1126/science.6823561 · Cited by 4,914
Autophagy and Viruses: Adversaries or Allies?
Dong, X., & Levine, B. (2013) · Journal of Innate Immunity · doi:10.1159/000346388 · Cited by 4,444
Parkin is recruited selectively to impaired mitochondria and promotes their autophagy
Narendra, D., Tanaka, A., Suen, D.-F., & Youle, R. J. (2008) · The Journal of Cell Biology · doi:10.1083/jcb.200809125 · Cited by 4,026
Self-citationChronic systemic pesticide exposure reproduces features of Parkinson's disease
Betarbet, R. S., Sherer, T., MacKenzie, G. M., Garcia‐Osuna, M., Panov, A. V., & Greenamyre, J. T. (2000) · Nature Neuroscience · doi:10.1038/81834 · Cited by 3,770
Mitochondrial Fission, Fusion, and Stress
Youle, R. J., & van der Bliek, A. M. (2012) · Science · doi:10.1126/science.1219855 · Cited by 3,674
Self-citationHereditary 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
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Self-citationFission and selective fusion govern mitochondrial segregation and elimination by autophagy
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Luthra, N. S., Clow, A., & Corcos, D. M. (2022) · Brain Sciences · doi:10.3390/brainsci12121695 · Cited by 20
Li, X., Initiative, O. B. O. A. D. N., Chu, S.-G., Shen, X.-N., Hou, X.-H., Xu, W., Ou, Y.-N., Dong, Q., Tan, L., & Yu, J.-T. (2019) · Aging · doi:10.18632/aging.102435 · Cited by 7
Metadata
- Authors
- Pickrell, A. M., & Youle, R. J.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Youle, Richard J.
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2015-01
- Volume
- 85
- Issue
- 2
- Pages
- 257-273
- ISSN
- 0896-6273 (ISSN-L)
- PMC
- PMC4764997
- OpenAlex
- W2082425146
- Cited by
- 2,310
- References
- 212
- Citations by year
- 2026: 268 · 2025: 234 · 2024: 177 · 2023: 175 · 2022: 228 · 2021: 261 · 2020: 239 · 2019: 197 · 2018: 178 · 2017: 174 · 2016: 123 · 2015: 54
- FWCI
- 23.21
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of General Medical Sciences
- National Institute of Neurological Disorders and Stroke (Z01NS002859)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Receptors and Signaling
- Keywords
- PINK1, Parkin, Parkinson's disease, mitochondrial quality control, mitochondrial damage, E3 ubiquitin ligase, selective autophagy, mitophagy, autosomal recessive parkinsonism, mitochondrial outer membrane
- MeSH terms
- PTEN-Induced Putative Kinase, Humans, Mitochondria, Parkinson Disease, Protein Kinases, Parkinsonian Disorders, Ubiquitin-Protein Ligases, Proteolysis, Mitophagy
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