Literature DB >> 16757807

Role of glutamine deamidation in neurodegenerative diseases associated with triplet repeat expansions: a hypothesis.

Qurratulain Hasan1, Ravindra Varma Alluri, Pragna Rao, Yog Raj Ahuja.   

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.

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Year:  2006        PMID： 16757807

Source DB:  PubMed          Journal:  J Mol Neurosci        ISSN： 0895-8696            Impact factor:   3.444


  28 in total

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Journal:  Hum Mol Genet       Date:  2000-01-01       Impact factor: 6.150

Review 7.  The neuropathology of CAG repeat diseases: review and update of genetic and molecular features.

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8.  Analysis of CAG repeats in SCA1, SCA2, SCA3, SCA6, SCA7 and DRPLA loci in spinocerebellar ataxia patients and distribution of CAG repeats at the SCA1, SCA2 and SCA6 loci in nine ethnic populations of eastern India.

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Journal:  Hum Genet       Date:  2000-06       Impact factor: 4.132

9.  Presymptomatic analysis of spinocerebellar ataxia type 1 (SCA1) via the expansion of the SCA1 CAG-repeat in a large pedigree displaying anticipation and parental male bias.

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Journal:  Hum Mol Genet       Date:  1993-12       Impact factor: 6.150

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Journal:  Science       Date:  1993-10-29       Impact factor: 47.728
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  3 in total

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Journal:  J Mol Neurosci       Date:  2014-10-12       Impact factor: 3.444

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  3 in total

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