ArticleBioMed research international2014
Alternative splicing generates different parkin protein isoforms: evidences in human, rat, and mouse brain.
Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Review
- Additional feedforward mechanism of Parkin activation via binding of phospho-UBL and RING0 ineLife · 2024Article
- Review
- Review
- Article
- WT1 Alternative Splicing: Role of Its Isoforms in Neuroblastoma.Journal of molecular neuroscience : MN · 2017Review
- Copy number variability in Parkinson's disease: assembling the puzzle through a systems biology approach.Human genetics · 2017Review
- Parkin Deficiency Reduces Hippocampal Glutamatergic Neurotransmission by Impairing AMPA Receptor Endocytosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- A customized high-resolution array-comparative genomic hybridization to explore copy number variations in Parkinson's disease.Neurogenetics · 2016Article
- Proteomic Analysis of Parkin Isoforms Expression in Different Rat Brain Areas.The protein journal · 2016Article
- Changes in the expression of splicing factor transcripts and variations in alternative splicing are associated with lifespan in mice and humans.Aging cell · 2016Article
- Genetics in Parkinson disease: Mendelian versus non-Mendelian inheritance.Journal of neurochemistry · 2016Review
- In Silico Analysis of SNPs inAdvances in bioinformatics · 2016Article
- Splicing: is there an alternative contribution to Parkinson's disease?Neurogenetics · 2015Review
- Expression pattern of parkin isoforms in lung adenocarcinomas.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Article
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5 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Parkinson protein 2, E3 ubiquitin protein ligase (PARK2) gene mutations are the most frequent causes of autosomal recessive early onset Parkinson's disease and juvenile Parkinson disease. Parkin deficiency has also been linked to other human pathologies, for example, sporadic Parkinson disease, Alzheimer disease, autism, and cancer. PARK2 primary transcript undergoes an extensive alternative splicing, which enhances transcriptomic diversification. To date several PARK2 splice variants have been identified; however, the expression and distribution of parkin isoforms have not been deeply investigated yet. Here, the currently known PARK2 gene transcripts and relative predicted encoded proteins in human, rat, and mouse are reviewed. By analyzing the literature, we highlight the existing data showing the presence of multiple parkin isoforms in the brain. Their expression emerges from conflicting results regarding the electrophoretic mobility of the protein, but it is also assumed from discrepant observations on the cellular and tissue distribution of parkin. Although the characterization of each predicted isoforms is complex, since they often diverge only for few amino acids, analysis of their expression patterns in the brain might account for the different pathogenetic effects linked to PARK2 gene mutations.
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