Fig. 1From: Molecular mechanisms of cisplatin-induced nephrotoxicity: a balance on the knife edge between renoprotection and tumor toxicityP53 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 transporterBack to article page