High impact information on Slc25a10

• Identification of dicarboxylate carrier Slc25a10 as malate transporter in de novo fatty acid synthesis [1].
• We have reported an Slc25a10 increase in white adipose tissue in obese mouse models and a decrease in a fasted mouse model using expression profiles [1].
• Furthermore, suppression of Slc25a10 decreased triglyceride lipid accumulation in adipose-differentiated 3T3-L1 cells [1].
• We observed that inhibition of malate transport by Slc25a10 suppression significantly reduced the citrate transport from the mitochondria to the cytosol [1].
• Next, we examined the effect of Slc25a10 suppression by small interfering RNA on citrate transport in the lipogenic cell lines HepG2 and 3T3-L1 [1].

Anatomical context of Slc25a10

• On the other hand, treatments that lead to a hyperpolarization of the mitochondrial membrane, such as overexpression of the mitochondrial dicarboxylate carrier result in increased ROS formation and decreased insulin sensitivity, even under normoglycemic conditions [2].
• It was found that the drug phenylsuccinate, which inhibits the mitochondrial dicarboxylate carrier as well as biosynthesis of neurotransmitter glutamate, inhibits swelling-induced taurine release both in vivo and in cultured cells [3].

Associations of Slc25a10 with chemical compounds

• We also found that suppression of Slc25a10 down-regulated the lipogenic pathway, indicated by decreases in ACC1 expression and malonyl-CoA level [1].

References