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The GDH genes were deleted and the phenotypes of the knockout mutants were studied by growth characterisation, metabolomics, isotope labelling experiments, and by quantifying cofactors under various hyphae-inducing conditions

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Conclusions In summary, our findings provide new insights into the molecular mechanisms driving MRTK progression, highlighting YTHDF1 and GSTM2 as potential therapeutic targets for this aggressive pediatric renal tumor