Uptake of citrate by human NaCT is driven by a sodium gradient. Its sodium-substrate coupling mechanism is unclear. Sauer et al. determined cryo-EM structures of the protein in apo, in sodium, and in ...

Lipid transfer proteins organize intracellular lipid distribution. Here, the authors show that seemingly redundant phospholipid transfer proteins have distinct acyl chain preferences, and suggest that their tissue-specific expression levels and phosphorylation fine-tune membrane composition.

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Thiopurines are widely used drugs whose activity depends on cellular metabolism. Here, the authors develop chemical tools to remove NUDT5 and show that protein loss, but not inhibition, alters drug re...

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Abstract. The divalent anion sodium symporter (DASS) family mediates the uptake of Krebs cycle intermediates and sulfate, and influences adiposity, insulin

This publication highlight is part of the SBGrid Communities Project focused on science education and demonstrating how structural biology…

Citrate is a key metabolic intermediate that regulates both glycolysis and lipid metabolism. While most citrate is produced in mitochondria, some is imported from the bloodstream by the SLC13 family o...

Spinster homolog 2 (SPNS2) exports sphingosine-1- 26 phosphate (S1P) out of cells. Here, the authors show that SPNS2 has antiporter-like activity, exporting S1P while importing glucose, revealing a me...

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The adult muscle-type nicotinic acetylcholine receptor (AChR) is essential for neuromuscular transmission but is difficult to produce due to the requirement for coordinated subunit assembly. Here, we ...

Cationic amino acids are essential to protein synthesis and cellular signaling. Here, authors determine the structure of the cationic amino acid transporter 1 and determined how it is co-opted as a re...

Ahead of her 85th birthday, Jane Richardson, Professor of Biochemistry at Duke University, discussed her life in science from making her own telescope to developing the ribbon diagrams for the 3D stru...

Ramdas et al. propose renaming ‘congenital myasthenic syndrome’ as ‘genetic myasthenic syndrome’. They argue that ‘congenital’ misleadingly implies neonata