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Mouse and other rodent models of C to U RNA editing.

Authors
  • Blanc, Valerie
  • Davidson, Nicholas O
Type
Published Article
Journal
Methods in Molecular Biology
Publication Date
Jan 01, 2011
Volume
718
Pages
121–135
Identifiers
DOI: 10.1007/978-1-61779-018-8_7
PMID: 21370045
Source
Medline
License
Unknown

Abstract

Substitutional RNA editing represents an important posttranscriptional enzymatic pathway for increasing genetic plasticity by permitting production of different translation products from a single genomically encoded template. One of the best-characterized examples in mammals is C to U deamination of the nuclear apolipoprotein B (apoB) mRNA. ApoB mRNA undergoes a single, site-specific cytidine deamination event yielding an edited transcript that results in tissue-specific translation of two distinct isoforms, referred to as apoB100 and apoB48. Tissue- and site-specific cytidine deamination of apoB mRNA is mediated by an incompletely characterized holoenzyme containing a minimal core complex consisting of an RNA-specific cytidine deaminase, Apobec-1 and a requisite cofactor, apobec-1 complementation factor (ACF). The underlying biochemical and genetic mechanisms regulating tissue-specific apoB mRNA editing have been accelerated through development and characterization of physiological rodent models as well as knockout and transgenic animal strains.

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