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Biology subjects

Tavoulari, S.

Publications and source records attributed to Tavoulari, S..

2 recordsLinked to original sources

Key features of inhibitor binding to the human mitochondrial pyruvate carrier hetero-dimer

The mitochondrial pyruvate carrier (MPC) has emerged as a promising drug target for metabolic disorders, including non-alcoholic steatohepatitis and diabetes, metabolically dependent cancers and neurodegenerative diseases. Human MPC is a protein complex, but the composition of its active form is debated and the mechanisms of transport and inhibition are not resolved. We have recombinantly expressed and purified the human hetero-complex MPC1L/MPC2 and demonstrate that it is a functional hetero-dimer, like the yeast MPC hetero-dimers. Unlike the latter, human MPC1L/MPC2 binds the known inhibitors with high potencies. We identify the essential chemical features shared between these structurally diverse inhibitors and demonstrate that high affinity binding is not attributed to covalent bond formation with MPC cysteines, as previously thought. We also identify 14 new inhibitors of MPC, one outperforming the most potent compound UK5099 by tenfold. Two of them are the commonly prescribed drugs entacapone and nitrofurantoin, suggesting possible off-target mechanisms associated with their adverse effects. This work advances our understanding of MPC inhibition and will accelerate the development of clinically relevant MPC modulators.

molecular biology↗

Structural elements required for coupling ion and substrate transport in the neurotransmitter transporter homolog LeuT.

The coupled transport of ions and substrates allows transporters to accumulate substrates using the energy in transmembrane ion gradients and electrical potentials. During transport, conformational changes that switch accessibility of substrate and ion binding sites from one side of the membrane to the other must be controlled so as to prevent uncoupled movement of ions or substrates. In the Neurotransmitter:Sodium Symporter (NSS) family, Na+ stabilizes the transporter in an outward-open state, thus decreasing the likelihood of uncoupled Na+ transport. In a step essential for coupled transport, substrate binding must overcome the effect of Na+, allowing intracellular substrate and Na+ release from an inward-open state. However, it is unclear which specific elements of the protein mediate this conformational response to substrate binding. Previously, we showed that in the prokaryotic NSS transporter LeuT, the effect of Na+ on conformation occurs at the Na2 site, where it influences conformation by fostering interaction between two domains of the protein (JBC 291: 1456, 2016). Here, we identify a conserved tyrosine residue in the substrate binding site required for substrate to enable conversion to inward-open states by establishing an interaction between the two transporter domains. We further identify additional interactions between the two transporter domains in the extracellular pathway that are required. Together with our previous work on the conformational effect of Na+, these results identify mechanistic components underlying ion-substrate coupling in NSS transporters.

biochemistry↗