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We use these results as a starting point to identify GAPDH as a neutrophil-intrinsic NET-suppressor mechanism and to investigate the molecular mechanisms by which GAPDH inhibition regulates neutrophil function

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Consequently, failure to convert RanGTP to RanGDP, for example, due to RanGAP depletion, is predicted to result in an accumulation of RanGTP in the cytoplasm and a shift in the ratio of nuclear to cytoplasmic total Ran protein [38]