Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10801985 | Biochimica et Biophysica Acta (BBA) - Molecular Cell Research | 2015 | 14 Pages |
Abstract
There are substantial differences regarding the cause of sensitivity and mechanisms of DDR between tubular and glomerular cells following platinum injury. CisPt is the most potent stimulator of the DDR. We hypothesize that specific DNA adducts and thereby forcefully activated pro-toxic DDR mechanisms contribute to the exceptionally high acute nephrotoxicity of CisPt.
Keywords
centromere protein FXIAPCSBChk1CisptRPAAPGγH2AXGPGMMRERK2Bcl2Mrp2DSBsDAPICTR1CHK2TC-NERGAPDHXPANRK-52E cellsNrf2IC50DDRXPGATRCenp-F3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide4′,6-diamidino-2-phenylindol5-ethynyl-2′-deoxyuridineataxia telangiectasia mutatedB-cell CLL/lymphoma 2DNA double-strand breaksNEREdUMTTNormal tissue damageOxaliplatincheckpoint kinase 1checkpoint kinase 2BaxTranscription-coupled nucleotide excision repairnucleotide excision repairmismatch repairATMcisplatinNF-E2-related factor 2Inhibitory Concentration 50%X-linked inhibitor of apoptosisNephrotoxicityDNA damage responseBCL2-associated X proteinPlatinumERCC1Carboplatinglyceraldehyde-3-phosphate dehydrogenase
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Authors
Katharina Krüger, Jürgen Thomale, Nikolina StojanoviÄ, Maja Osmak, Christian Henninger, Stefanie Bormann, Gerhard Fritz,