ArticleJournal of molecular neuroscience : MN2006
Role of glutamine deamidation in neurodegenerative diseases associated with triplet repeat expansions: a hypothesis.
Article in Journal of molecular neuroscience : MN, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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Who cites it
6 citing papers in PubMed.
- Post-translational modifications of pancreatic fluid proteins collected via the endoscopic pancreatic function test (ePFT).Journal of proteomics · 2013Trial
- Expanding the Chemoproteomic Toolkit to Asparagine and Glutamine.ACS chemical biology · 2026Article
- Article
- Molecular spectrum and allelic frequency of different subtypes (1, 2, 3, 6 and 7) of Spinocerebellar ataxia in the Indian population.Intractable & rare diseases research · 2019Article
- Role of dynamic and mitochondrial mutations in neurodegenerative diseases with ataxia: lower repeats and LNAs at multiple loci as alternative pathogenesis.Journal of molecular neuroscience : MN · 2014Article
- Protein truncation as a common denominator of human neurodegenerative foldopathies.Molecular neurobiology · 2013Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathological expansion of unstable trinucleotide repeats is known to cause neurodegenerative diseases. Trinucleotide repeat expansions might prove to be pathological through a variety of mechanisms, including alteration of DNA structure, transcription, RNA-protein interaction, and altered protein conformations/interactions. Deamidation of human proteins have been shown to regulate some time-dependent biological processes such as development and aging. In this paper we hypothesize the possible role of glutamine deamidation as a signaling event in the pathogenesis of neurodegenerative diseases associated with triplet repeat expansion.
Indexed as
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Registered trials
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