ApoB100 is produced in the liver while apoB48 is produced in the intestine. The mechanism that allows the formation of apoB48 instead of apoB100 involves
a) Capping
b) RNA splicing
c) RNA editing
d) Post-translational modification
e) homologous genes
In the intestines, there's a C to a U deamination that creates an early stop codon that truncates the protein at 48% of the normal length. I don't think it has anything to do with an early splice site.
