Disease relevance of Slc25a1

• These results suggest that hypothyroidism affects TCC expression at both the transcriptional and post-transcriptional levels [1].
• Renal tubular citrate transport is accomplished by electrogenic Na(+) coupled dicarboxylate transporter NaDC-1, a carrier subjected to regulation by acidosis [2].
• Hypocitraturia induced by citrate transport disturbance is known to be involved in nephrolithiasis development [3].
• Effect of vitamin D deficiency on D-glucose and citrate transport in rat renal basolateral membrane vesicles [4].
• The rate of citrate transport was greatly reduced in rats during both the proliferative phase (3 days after the lead nitrate administration) and the involutive phase (5 days after the metal injection), which follows hepatic hyperplasia and corresponds to the peak of hepatocyte apoptosis [5].

High impact information on Slc25a1

• The tricarboxylate carrier (TCC), also known as citrate carrier, is an integral protein of the mitochondrial inner membrane [1].
• Hypothyroidism reduces tricarboxylate carrier activity and expression in rat liver mitochondria by reducing nuclear transcription rate and splicing efficiency [1].
• Hypothyroidism did not influence TCC mRNA stability [1].
• Furthermore, we found that the ratio of polyadenylated/unpolyadenylated TCC RNA as well as the length of the TCC RNA poly(A) tail were similar in both euthyroid and hypothyroid rats [1].
• Blocking the tricarboxylate anion exchange carrier with the citrate transport inhibitor 1,2,3-benzenetricarboxylate restores the ability of tumor 3924A mitochondria to respire with pyruvate or citrate [6].

Biological context of Slc25a1

• Different dietary fatty acids have dissimilar effects on activity and gene expression of mitochondrial tricarboxylate carrier in rat liver [7].
• The tricarboxylate carrier (TCC), an integral protein of the mitochondrial inner membrane, transports mitochondrial acetyl-CoA into the cytosol, where lipogenesis occurs [7].
• Molecular toxicology of (-)-erythro-fluorocitrate: selective inhibition of citrate transport in mitochondria and the binding of fluorocitrate to mitochondrial proteins [8].
• As a consequence of these last two points, the rate of citrate transport by the carrier is much higher when it operates in exchange with another substrate than when it operates in net uniport [9].
• The tissue and substrate specificity, the inhibitor sensitivity and the kinetic properties of citrate transport in liposomes are similar to those described for the citrate transport in mitochondria [10].

Anatomical context of Slc25a1

• In this study, we characterized the presequence of the citrate carrier (CIC, tricarboxylate carrier) of rat liver mitochondria [11].
• These results are consistent with an arrangement of the tricarboxylate carrier monomer into an even number of transmembrane segments, with the N- and C-termini protruding toward the cytosol [12].
• The N- and C-termini of the tricarboxylate carrier are exposed to the cytoplasmic side of the inner mitochondrial membrane [12].
• Regulation of citrate transport and pyruvate dehydrogenase in rat kidney cortex mitochondria by bicarbonate [13].
• BACKGROUND: Electrophysiological characterization of normal human prostate epithelial cells showed exogenous trivalent citrate transport (release) to be K(+)-dependent [14].

Associations of Slc25a1 with chemical compounds

• Phosphoenolpyruvate, which is a substrate for the tricarboxylate carrier, inhibited GSH uptake, but this was due to induction of the membrane permeability transition and not to competition for uptake [15].
• 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 [16].
• Cardiolipin protects against the inhibition by Br-daunomycin and the reconstituted citrate transport activity depends upon the ratio of cardiolipin/Br-daunomycin [17].
• We have now studied D-glucose and citrate transport into basolateral membrane vesicles prepared from kidney cortex of control and rachitic rats and the effect of 1,25-dihydroxyvitamin D3 on these transport systems was also investigated [4].
• The present studies evaluate the effect of lithium administration on tissue phosphate distribution, metabolites content in the kidneys and renal phosphate, 2-oxoglutarate and citrate transport in the presence and absence of db-cyclic AMP [18].

Other interactions of Slc25a1

• The objective was to further test the hypothesis that aluminum (Al) citrate transport across the blood-brain barrier is mediated by a monocarboxylate transporter (MCT) [19].

Analytical, diagnostic and therapeutic context of Slc25a1

• ELISA tests performed with intact and permeabilized rat-liver mitoplasts showed that both anti-N-terminal and anti-C-terminal antibodies bind only to the cytoplasmic surface of the inner membrane, indicating that both termini of the membrane-bound tricarboxylate carrier are exposed to the mitochondrial intermembrane space [12].
• Aluminum citrate transport across the blood-brain barrier was assessed in rats by in vivo microdialysis [20].

References