Deficit of p66ShcA restores redox-sensitive stress response program in cisplatin-induced acute kidney injury

Experimental and Molecular Pathology

Volumn 94, Issue 3, 2013, Pages 445-452

  Rattanavich, Rungwasee ^a   Plagov, Andrei ^a   Kumar, Dileep ^a   Rai, Partab ^a   Lederman, Rivka ^a   Salhan, Divya ^a   Vashistha, Himanshu ^b   Malhotra, Ashwani ^a   Meggs, Leonard G ^b   Singhal, Pravin C ^a  

^a DONALD AND BARBARA ZUCKER SCHOOL OF MEDICINE AT HOFSTRA NORTHWELL   (United States)

^b OCHSNER CLINIC FOUNDATION   (United States)

Author keywords

Acute kidney injury; Apoptosis; Cisplatinum; Oxidative stress; P66ShcA; Redox sensitive stress response program

Indexed keywords

CATALASE; CISPLATIN; MANGANESE SUPEROXIDE DISMUTASE; NITROGEN; PROTEIN BAX; PROTEIN P53; PROTEIN P66; PROTEIN P66SHCA; REGULATOR PROTEIN; SODIUM CHLORIDE; TRANSCRIPTION FACTOR FKHRL1; UNCLASSIFIED DRUG; UREA;

ACUTE KIDNEY FAILURE; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; CELL LYSATE; CELLULAR STRESS RESPONSE; CONTROLLED STUDY; FEMALE; HETEROZYGOTE; HISTOPATHOLOGY; IN VITRO STUDY; KIDNEY PARENCHYMA; KIDNEY PROXIMAL TUBULE; KIDNEY TUBULE CELL; KIDNEY TUBULE DISORDER; MALE; MOUSE; NONHUMAN; OXIDATION REDUCTION REACTION; PROTEIN DEPLETION; PROTEIN EXPRESSION; PROTEIN FUNCTION; PROTEIN PHOSPHORYLATION; PROTEIN PROTEIN INTERACTION; SINGLE DRUG DOSE; UREA NITROGEN BLOOD LEVEL;

EID: 84876319793     PISSN: 00144800     EISSN: 10960945     Source Type: Journal    
DOI: 10.1016/j.yexmp.2013.03.001     Document Type: Article

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