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high glutathione circadian rhythm An integrative multi-omics analysis leveraging Mendelian randomization and subsequent experimental validation prioritizes S-transferase mu 5 (GSTM5) as a genomic stability-related gene and a therapeutic vulnerability to PLK1 inhibition in Molecular regulations of circadian rhythm

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doi: 10.1073/pnas.95.20.11715

high glutathione circadian rhythm An integrative multi-omics analysis leveraging Mendelian randomization and subsequent experimental validation prioritizes S-transferase mu 5 (GSTM5) as a genomic stability-related gene and a therapeutic vulnerability to PLK1 inhibition in Molecular regulations of circadian rhythm

Il est fondamental pour lhomostasie cellulaire, impliqu dans le mtabolisme des nutriments, la dfense antioxydante, la synthse de lADN et des protines, et la rgulation du cycle cellulaire

high glutathione circadian rhythm An integrative multi-omics analysis leveraging Mendelian randomization and subsequent experimental validation prioritizes S-transferase mu 5 (GSTM5) as a genomic stability-related gene and a therapeutic vulnerability to PLK1 inhibition in Molecular regulations of circadian rhythm

Andrews McMeel Publishing

high glutathione circadian rhythm An integrative multi-omics analysis leveraging Mendelian randomization and subsequent experimental validation prioritizes S-transferase mu 5 (GSTM5) as a genomic stability-related gene and a therapeutic vulnerability to PLK1 inhibition in Molecular regulations of circadian rhythm

Understanding these metabolic reprogramming processessuch as PDK4-mediated pyruvate dehydrogenase inhibition and PKM2/PKM1 isoform switchingcould identify novel therapeutic targets by regulating key pathways like Anaphase-promoting complex/cyclosome and its coactivator Cdh1 (APC/C-Cdh1)-dependent PFKFB3 stabilization or pentose phosphate pathway activation

high glutathione circadian rhythm An integrative multi-omics analysis leveraging Mendelian randomization and subsequent experimental validation prioritizes S-transferase mu 5 (GSTM5) as a genomic stability-related gene and a therapeutic vulnerability to PLK1 inhibition in Molecular regulations of circadian rhythm

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