Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:6.4.1.2 (
acetyl-CoA carboxylase
)
2,876
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Because of certain similarities between
acetyl-CoA carboxylase
(
ACC
) and tubulin, and the recent demonstration of the ADP-ribosylation of tubulin by cholera toxin, we have investigated a potential role for ADP-ribosylation in the regulation of
ACC
activity. Incubation of purified rat liver
ACC
with cholera toxin in the presence of millimolar concentrations of [adenylate-32P]NAD results in a time-dependent incorporation of ADP-ribose into
ACC
of greater than 2 mol/mol of enzyme subunit, accompanied by a marked inactivation of enzyme activity. This effect is not mimicked by pertussis toxin, ADP-ribose, or ribose 5-phosphate. Incubation of labeled
ACC
with snake
venom phosphodiesterase
and alkaline hydrolysis release 32P-products tentatively identified by high-performance liquid chromatography as 5'-[32P]AMP and [32P]ADP-ribose, respectively. These data are consistent with a mono-ADP-ribosylation of
ACC
catalyzed by cholera toxin. Phosphodiesterase treatment of inactivated
ACC
partially restores enzyme activity. The effects of ADP-ribosylation of
ACC
are expressed both as a decrease in the enzyme Vmax and as an increase in the apparent Ka for citrate. These results suggest that
ACC
might be a substrate for endogenous ADP-ribosyltransferases and that this covalent modification could be an important regulatory mechanism for the modulation of fatty acid synthesis in vivo.
...
PMID:Regulation of acetyl-CoA carboxylase by ADP-ribosylation. 287 58
