ReviewCerebellum (London, England)2007
Transcriptional malfunctioning of heat shock protein gene expression in spinocerebellar ataxias.
Review in Cerebellum (London, England), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- Planar cell polarity geneEMBO reports · 2018Article
- Assessing a peptidylic inhibitor-based therapeutic approach that simultaneously suppresses polyglutamine RNA- and protein-mediated toxicities in patient cells and Drosophila.Disease models & mechanisms · 2016Article
- Allele-specific silencing of mutant Ataxin-7 in SCA7 patient-derived fibroblasts.European journal of human genetics : EJHG · 2014Article
- Past, present and future therapeutics for cerebellar ataxias.Current neuropharmacology · 2010Article
- The cerebellum, cerebellar disorders, and cerebellar research--two centuries of discoveries.Cerebellum (London, England) · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Among the various dominantly-inherited spinocerebellar ataxias (SCAs), at least seven of them belong to the polyglutamine disease group and are caused by glutamine-coding CAG triplet repeat expansion. The expanded coding CAG repeat translates into a polyglutamine stretch in the disease protein, which leads to late-onset and progressive neurodegeneration. Expanded polyglutamine adopts a misfolded protein conformation, and is itself a cellular stressor which induces robust heat shock response (HSR). Under polyglutamine stress, heat shock proteins (Hsps) are produced in neurons to assist refolding and/or promote the degradation of misfolded proteins. Along with the progressive nature of polyglutamine degeneration, a gradual decline of HSR in degenerating neurons was observed. Such kind of reduction can be observed in a large family of hsp gene expression, including hsp22, 26, 27, and 70. This underscores an intimate relationship between the inducibility of hsp gene expression and the disease progression. In this review, we describe the current understandings of hsp gene dysregulation in polyglutamine disease.
Indexed as
Identifiers
17510910What 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.