ArticleCurrent genomics2014
Increasing the Coding Potential of Genomes Through Alternative Splicing: The Case of PARK2 Gene.
Article in Current genomics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
- Review
- Parkin deficiency impairs female fertility, oocyte development, fertilization and mitochondrial function in mice.npj aging · 2026Article
- Shifts in isoform usage underlie transcriptional differences in regulatory T cells in type 1 diabetes.Communications biology · 2023Article
- Autophagy regulation by RNA alternative splicing and implications in human diseases.Nature communications · 2022Review
- Review
- The role of DNA methylation in the pathogenesis of type 2 diabetes mellitus.Clinical epigenetics · 2020Review
- Article
- Article
- PARK2 inhibits osteosarcoma cell growth through the JAK2/STAT3/VEGF signaling pathway.Cell death & disease · 2018Article
- 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
- 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
- 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
- Burden analysis of rare microdeletions suggests a strong impact of neurodevelopmental genes in genetic generalised epilepsies.PLoS genetics · 2015Article
- Aberrant transcriptional regulation could explain phenotypic variability in autosomal recessive polycystic kidney disease.Journal of molecular medicine (Berlin, Germany) · 2014Article
- Alternative splicing generates different parkin protein isoforms: evidences in human, rat, and mouse brain.BioMed research international · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The completion of the Human Genome Project aroused renewed interest in alternative splicing, an efficient and widespread mechanism that generates multiple protein isoforms from individual genes. Although our knowledge about alternative splicing is growing exponentially, its real impact on cellular life is still to be clarified. Connecting all splicing features (genes, splice transcripts, isoforms, and relative functions) may be useful to resolve this tangle. Herein, we will start from the case of a single gene, Parkinson protein 2, E3 ubiquitin protein ligase (PARK2), one of the largest in our genome. This gene is implicated in the pathogenesis of autosomal recessive juvenile Parkinsonism and it has been recently linked to cancer, leprosy, autism, type 2 diabetes mellitus and Alzheimer's disease. PARK2 primary transcript undergoes an extensive alternative splicing, which enhances transcriptomic diversification and protein diversity in tissues and cells. This review will provide an update of all human PARK2 alternative splice transcripts and isoforms presently known, and correlate them to those in rat and mouse, two common animal models for studying human disease genes. Alternative splicing relies upon a complex process that could be easily altered by both cis and trans-acting mutations. Although the contribution of PARK2 splicing in human disease remains to be fully explored, some evidences show disruption of this versatile form of genetic regulation may have pathological consequences.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.