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Here, we uncover a profound niche-specific metabolic vulnerability in CNS-resident ALL cells, characterised by an obligate reliance on LRP8-mediated selenium uptake to sustain selenocysteine biosynthesis and GPX4 activity under profound glutathione limitation

A key component in this signaling cascade is phospholipase C (PLC), a crucial enzyme that, according to some scientific hypotheses, may facilitate the production of inositol triphosphate (IP3) and diacylglycerol (DAG)

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Here we show by X-ray crystallography that the ligandin binding site in human pi class GST P1-1 occupies part of one of the substrate binding sites