High impact information on NSC 401092

• The carrier, after reconstitution in phospholipid vesicles, catalyzed the exchange of [14C]citrate against citrate, malate, and threo-D8-isocitrate and was inhibited by the specific tricarboxylate carrier inhibitor 1,2,3-benzenetricarboxylic acid [1].
• The specific citrate transport activity of this preparation is not significantly different from that measured in mitochondria and it is inhibitable by 1,2,3-benzenetricarboxylic acid [2].
• Decarboxylation of benzene-1,2,3-tricarboxylic acid to phthalate (VIII), as well as further oxidation of the latter, would connect both routes with the central metabolism [3].
• Monooxygenation of this ketone to the quinone and subsequent hydrolysis generates naphthalene-1,8-dicarboxylic acid (IV), which is further degraded via benzene-1,2,3-tricarboxylic acid (III) [3].
• Regioselective methylation of hemimellitic acid in basic MeOH yields the title 2-methyl ester, C(10)H(8)O(6), of the parent acid [4].

Biological context of NSC 401092

• When n-butylmalonate is added to slow down the flux of glycolytic reducing equivalents to the respiratory chain via the malate-aspartate shuttle, benzenetricarboxylic acid or hydroxycitrate promotes an ATP-driven reversal of electron transfer [5].

Gene context of NSC 401092

• It has been discovered that 1,2,3-benzenetricarboxylic acid and some 5-substituted derivatives are specific and competitive inhibitors of the mitochondrial tricarboxylate carrier [6].

References