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Description
Of particular interest is the increased expression of GLUT1 on erythrocytes as a compensatory mechanism for vitamin recycling in mammals that cannot synthesize vitamin C
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However, wild-type p53 could delay induction of ferroptosis by regulating its transcriptional target CDKN1A (encoding p21)
M., Kratochvl, L., Flegr, J., Weston, K
