The DOI matches its Crossref record; 46 of the 49 references it cites were found in a registry or an index.
PINK1 protein in normal human brain and Parkinson's disease
Abstract
Parkinson's disease is a common incurable neurodegenerative disease whose molecular aetiology remains unclear. The identification of Mendelian genes causing rare familial forms of Parkinson's disease has revealed novel proteins and pathways that are likely to be relevant in the pathogenesis of sporadic Parkinson's disease. Recently, mutations in a novel gene, PINK1, encoding a 581 amino acid protein with both mitochondrial targeting and serine/threonine kinase domains, were identified as a cause of autosomal recessive parkinsonism. This provided important evidence for the role of the mitochondrial dysfunction and kinase pathways in neurodegeneration. In this study, we report the first characterization of the PINK1 protein in normal human and sporadic Parkinson's brains, in addition to Parkinson's cases with heterozygous PINK1 mutations. The possible role of the PINK1 protein was also assessed in a number of neurodegenerative diseases characterized by proteinaceous inclusions. For these studies, rabbit polyclonal antibodies were raised against two peptide sequences within the N-terminal hydrophilic loops of PINK1 protein. Using immunohistochemistry and western blotting we were able to demonstrate that PINK1 is a ubiquitous protein expressed throughout the human brain and it is found in all cell types showing a punctate cytoplasmic staining pattern consistent with mitochondrial localization. Fractionation studies of human and rat brain confirm that PINK1 is localized to the mit…
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“PINK1 is expressed ubiquitously in neurons throughout the human brain [59, 60].”
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 [60]
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Metadata
- Authors
- Gandhi, S.
- Affiliations
- UCL Queen Square Institute of Neurology (GB)
- Corresponding author
- Gandhi, S.
- ORCID
- Gandhi, S.
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2006-07-01
- Volume
- 129
- Issue
- 7
- Pages
- 1720-1731
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- OpenAlex
- W2131641631
- Cited by
- 342
- References
- 49
- Citations by year
- 2026: 6 · 2025: 8 · 2024: 11 · 2023: 4 · 2022: 8 · 2021: 11 · 2020: 9 · 2019: 12 · 2018: 9 · 2017: 10 · 2016: 14 · 2015: 12 · 2014: 17 · 2013: 22 · 2012: 22
- FWCI
- 24.12
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- Wellcome Trust
- Parkinson's UK (G-4062)
- Cotton Research and Development Corporation
- Medical Research Council
- Reta Lila Weston Institute of Neurological Studies, UCL Queen Square Institute of Neurology,University College London
- Topics
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Receptors and Signaling
- Life Sciences › Neuroscience › Neurology › Neurological diseases and metabolism
- Keywords
- PINK1, Parkinson's disease, sporadic Parkinson's disease, mitochondrial dysfunction, Lewy bodies, mitochondrial localization, neurodegeneration, autosomal recessive parkinsonism, neurofibrillary tangles, alpha-synuclein inclusions, multiple system atrophy, progressive supranuclear palsy, corticobasal degeneration, Alzheimer's disease, serine/threonine kinase
- MeSH terms
- PTEN-Induced Putative Kinase, Alzheimer Disease, Animals, Brain, Carbonates, Female, Heterozygote, Humans, Immunoenzyme Techniques, Male, Middle Aged, Mitochondria, Mutation, Parkinson Disease, Protein Kinases, Submitochondrial Particles, Rats, Wistar, Multiple System Atrophy, Lewy Body Disease, Mitochondrial Membranes, Rats
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