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Fig. 1 | Journal of Biomedical Science

Fig. 1

From: Molecular mechanisms of cisplatin-induced nephrotoxicity: a balance on the knife edge between renoprotection and tumor toxicity

Fig. 1

P53 signaling pathways leading to tubular cell apoptosis after cisplatin treatment. By transcriptional regulation, nuclear p53 may activate proapoptotic genes, such as PUMA-α, caspases, PIDD, and ER-iPLA2, may suppress antiapoptotic genes, including p21 and TauT. In the absence of transcription, p53 may induce apoptosis via interactions with Bcl-2 family proteins in mitochondria and/or cytosol. Abbreviations: Bcl-2: B-cell lymphoma 2; Bcl-xL: B-cell lymphoma-extra large; Bax: Bcl-2-associated X protein; Bak: Bcl-2 homologous antagonist killer; PUMA-α: p53 upregulated modulator of apoptosis; PIDD: p53-induced protein with a death domain; ER-iPLA2: Ca2+-independent phospholipase A2; Cdk2: Cyclin-dependent kinase complex; TauT: taurine transporter

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