TY - JOUR
T1 - Role of glutamine deamidation in neurodegenerative diseases associated with triplet repeat expansions
T2 - A hypothesis
AU - Hasan, Qurratulain
AU - Alluri, Ravindra Varma
AU - Rao, Pragna
AU - Ahuja, Yog Raj
PY - 2006/5
Y1 - 2006/5
N2 - 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.
AB - 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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U2 - 10.1385/JMN:29:1:29
DO - 10.1385/JMN:29:1:29
M3 - Article
C2 - 16757807
AN - SCOPUS:33744948924
SN - 0895-8696
VL - 29
SP - 29
EP - 33
JO - Journal of Molecular Neuroscience
JF - Journal of Molecular Neuroscience
IS - 1
ER -
