Inefficient A-to-I RNA editing and ALS

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[Inefficient A-to-I RNA editing and ALS].

GluR2 is a subunit of the AMPA receptor, and failure of naturally occurring adenosine to inosine (A-to-I) conversion at its Q R site results in an increase of Ca influx through the AMPA receptor, thereby inducing exaggerated neuronal excitation. Indeed, mutant mice unable to edit this site die from status epilepticus. A-to-I conversion at this site is inefficient in the dying motor neurons of s...

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RNA Editing: An I for editing

In vitro editing in mammalian nuclear extracts reveals adenosine-to-inosine conversions in glutamate receptor messenger RNAs.

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The evolution and adaptation of A-to-I RNA editing

Adenosine-to-inosine (A-to-I) RNA editing is an important post-transcriptional modification that affects the information encoded from DNA to RNA to protein. RNA editing can generate a multitude of transcript isoforms and can potentially be used to optimize protein function in response to varying conditions. In light of this and the fact that millions of editing sites have been identified in man...

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Is abundant A-to-I RNA editing primate-specific?

A-to-I RNA editing is common in all eukaryotes, and is associated with various neurological functions. Recently, A-to-I editing was found to occur frequently in the human transcriptome. In this article, we show that the frequency of A-to-I editing in humans is at least an order of magnitude higher than in the mouse, rat, chicken or fly genomes. The extraordinary frequency of RNA editing in huma...

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Adaptation of A-to-I RNA editing in Drosophila

Adenosine-to-inosine (A-to-I) editing is hypothesized to facilitate adaptive evolution by expanding proteomic diversity through an epigenetic approach. However, it is challenging to provide evidences to support this hypothesis at the whole editome level. In this study, we systematically characterized 2,114 A-to-I RNA editing sites in female and male brains of D. melanogaster, and nearly half of...

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ژورنال

عنوان ژورنال: Rinsho Shinkeigaku

سال: 2010

ISSN: 0009-918X,1882-0654

DOI: 10.5692/clinicalneurol.50.978