PMID:8626621

Citation	Hirano, K, Young, SG, Farese, RV Jr, Ng, J, Sande, E, Warburton, C, Powell-Braxton, LM and Davidson, NO (1996) Targeted disruption of the mouse apobec-1 gene abolishes apolipoprotein B mRNA editing and eliminates apolipoprotein B48. J. Biol. Chem. 271:9887-90
Abstract	A site-specific C to U editing reaction modifies nuclear apolipoprotein B100 (apoB100) mRNA, producing apolipoprotein B48 in the mammalian small intestine. This reaction is mediated by a multicomponent enzyme complex, which contains a catalytic subunit, Apobec-1. We have used gene targeting to disrupt mouse apobec-1 in order to establish its requisite importance in apoB mRNA editing and also, in view of its widespread tissue distribution in rodents, as a preliminary indication of other potential roles. Both heterozygous (apobec-1+/-) and homozygous (apobec-1-/-) gene-targeted mice appear healthy and fertile with no alterations in serum cholesterol or triglyceride concentrations. The apobec-1+/- mice demonstrated reduced levels of hepatic apoB mRNA editing. By contrast, levels of small intestinal apoB mRNA editing were indistinguishable in wild-type and apobec-1+/- animals, suggesting that Apobec-1 is expressed in limited quantities in the liver but not in the small intestine. The apobec-1-/- mice lacked detectable levels of Apobec-1 mRNA, expressed only unedited apoB mRNA in all tissues, and contained no apoB48 in their serum, demonstrating that there is no functional duplication of this gene.
Links	PubMed
Keywords	Animals; Apolipoprotein B-48; Apolipoproteins B/genetics; Arteriosclerosis/etiology; Base Sequence; Cytidine Deaminase/physiology; DNA Primers/chemistry; Intestine, Small/metabolism; Kidney/metabolism; Liver/metabolism; Mice; Mice, Knockout; Molecular Sequence Data; RNA Editing
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