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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>
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mRNA Editing: C to U Conversion
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