ReviewJournal of genetics2010
Modifiers and mechanisms of multi-system polyglutamine neurodegenerative disorders: lessons from fly models.
Review in Journal of genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 2 of them syntheses that pooled it.
What it found
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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.
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Who cites it
13 citing papers in PubMed, 2 syntheses or guidelines pooled it, 28 citations in OpenAlex.
- NeuroGeM, a knowledgebase of genetic modifiers in neurodegenerative diseases.BMC medical genomics · 2013Pooled it
- Identification of common genetic modifiers of neurodegenerative diseases from an integrative analysis of diverse genetic screens in model organisms.BMC genomics · 2012Pooled it
- Hsrω and Other lncRNAs in Neuronal Functions and Disorders inLife (Basel, Switzerland) · 2022Review
- Stress granules, RNA-binding proteins and polyglutamine diseases: too much aggregation?Cell death & disease · 2021Review
- Azadiradione ameliorates polyglutamine expansion disease in Drosophila by potentiating DNA binding activity of heat shock factor 1.Oncotarget · 2016Article
- Decreased O-linked GlcNAcylation protects from cytotoxicity mediated by huntingtin exon1 protein fragment.The Journal of biological chemistry · 2014Article
- From normal gait to loss of ambulation in 6 months: a novel presentation of SCA17.Cerebellum (London, England) · 2013Article
- Dysregulation of core components of SCF complex in poly-glutamine disorders.Cell death & disease · 2012Article
- Severe and rapidly progressing cognitive phenotype in a SCA17-family with only marginally expanded CAG/CAA repeats in the TATA-box binding protein gene: a case report.BMC neurology · 2012Article
- Probing mechanisms that underlie human neurodegenerative diseases in Drosophila.Annual review of genetics · 2012Review
- Drosophila models of proteinopathies: the little fly that could.Current pharmaceutical design · 2012Review
- In vivo effects of traditional Ayurvedic formulations in Drosophila melanogaster model relate with therapeutic applications.PloS one · 2012Article
- Forty years of the 93D puff of Drosophila melanogaster.Journal of biosciences · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polyglutamine (polyQ) diseases, resulting from a dynamic expansion of glutamine repeats in a polypeptide, are a class of genetically inherited late onset neurodegenerative disorders which, despite expression of the mutated gene widely in brain and other tissues, affect defined subpopulations of neurons in a disease-specific manner. We briefly review the different polyQ-expansion-induced neurodegenerative disorders and the advantages of modelling them in Drosophila. Studies using the fly models have successfully identified a variety of genetic modifiers and have helped in understanding some of the molecular events that follow expression of the abnormal polyQ proteins. Expression of the mutant polyQ proteins causes, as a consequence of intra-cellular and inter-cellular networking, mis-regulation at multiple steps like transcriptional and posttranscriptional regulations, cell signalling, protein quality control systems (protein folding and degradation networks), axonal transport machinery etc., in the sensitive neurons, resulting ultimately in their death. The diversity of genetic modifiers of polyQ toxicity identified through extensive genetic screens in fly and other models clearly reflects a complex network effect of the presence of the mutated protein. Such network effects pose a major challenge for therapeutic applications.
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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.