The best characterized case of C to U editing is in the intestinal apolipoprotein B transcript, where the editing event creates a premature translation stop codon and consequently leads to a shorter form of the protein. In the liver, C to U editing is important in the expression of specific isoforms of the apolipoprotein B enzyme. ApoB mRNA editing is a posttranscriptional, nuclear process that can be initiated after splicing, at the time of polyadenylation and is completed by the time pre-mRNA matures fully (reviewed by Blanc and Davidson, 2003).<BR>This editing event is a simple hydrolytic cytidine deamination to uridine, and is carried out by the Apobec-1 enzyme, along with the Apobec-1 complementing factor, ACF. The editing of apo-B mRNA involves the site-specific deamination of (C6666 to U), which converts codon 2153 from a glutamine codon, CAA, to a premature stop codon, UAA. As ACF is distributed in a variety of tissues, and these genes contain multiple family members, it is possible that editing events in additional targets will be found.<BR>The cis-acting regulatory elements for C to U editing include: 22 nt editing site within ApoB mRNA, 5’ tripartite motif with an enhancer element adjacent to the target cytidine, a spacer element and mooring sequence both 3’ to the cytidine (reviewed by Smith et al., 1997). The editing complex can be represented as:<BR>

http://purl.obolibrary.org/obo/HINO_0021089

The best characterized case of C to U editing is in the intestinal apolipoprotein B transcript, where the editing event creates a premature translation stop codon and consequently leads to a shorter form of the protein. In the liver, C to U editing is important in the expression of specific isoforms of the apolipoprotein B enzyme. ApoB mRNA editing is a posttranscriptional, nuclear process that can be initiated after splicing, at the time of polyadenylation and is completed by the time pre-mRNA matures fully (reviewed by Blanc and Davidson, 2003).
This editing event is a simple hydrolytic cytidine deamination to uridine, and is carried out by the Apobec-1 enzyme, along with the Apobec-1 complementing factor, ACF. The editing of apo-B mRNA involves the site-specific deamination of (C6666 to U), which converts codon 2153 from a glutamine codon, CAA, to a premature stop codon, UAA. As ACF is distributed in a variety of tissues, and these genes contain multiple family members, it is possible that editing events in additional targets will be found.
The cis-acting regulatory elements for C to U editing include: 22 nt editing site within ApoB mRNA, 5’ tripartite motif with an enhancer element adjacent to the target cytidine, a spacer element and mooring sequence both 3’ to the cytidine (reviewed by Smith et al., 1997). The editing complex can be represented as:

Pubmed12683974

Reactome, http://www.reactome.org

Pubmed11092837

Pubmed11072063

Pubmed12446660

mRNA Editing: C to U Conversion

http://purl.obolibrary.org/obo/NCBITaxon_9606

HINO:0021089

mRNA Editing: C to U Conversion

Reactome Database ID Release 4372200

ReactomeREACT_167

GENE ONTOLOGYGO:0016554

http://purl.obolibrary.org/obo/INO_0000021

http://purl.obolibrary.org/obo/HINO_0019848

http://purl.obolibrary.org/obo/HINO_0021092