Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.6.1.3 (ATPase)
 65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Structure-activity analyses of the effects of unsaturated fatty acids on the inhibition of gastric H+,K(+)-ATPase were carried out. Saturated fatty acids are poor inhibitors of H+,K(+)-ATPase, compared with unsaturated ones. Among the cis-unsaturated fatty acids with one double bond, there was an optimal carbon chain length for the inhibitory of the enzyme, and 10-nonadecenoic acid (C19:1) was the most potent inhibitor. The inhibitory activity was not altered by a change in the position of the double bond. The cis-fatty acids were more potent than the corresponding trans-fatty acids. Esterification of the acid moiety resulted in a decrease of the inhibitory activity. However, conversion of the acid moiety into alcohol and amide did not decrease the activity. These findings suggest that two moieties of unsaturated fatty acids are important in the interaction with the gastric H+,K(+)-ATPase, the carbon chain, which may have some hydrophobic interactions with the enzyme, and the terminal functional group (acid moiety), which may interact with hydrophilic interactions such as through hydrogen bonds with the enzyme.
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PMID:Structure-activity relationships of unsaturated long chain fatty acids in relation to the inhibition of gastric H+,K(+)-ATPase. 795 95