Role of reactive oxygen species (ROS) and JNKs in selenite-induced apoptosis in HepG2 cells

Cancer Biology and Therapy

Volumn 7, Issue 5, 2008, Pages 697-698

  Cherukuri, Durga P ^a,c   Nelson, Mark A ^b  

^a UNIVERSITY OF ARIZONA   (United States)

^b UNIVERSITY OF ARIZONA COLLEGE OF MEDICINE   (United States)

^c UNIVERSITY OF ARIZONA   (United States)

Author keywords

Apoptosis; HepG2; JNK; ROS; Selenite

Indexed keywords

REACTIVE OXYGEN METABOLITE; SELENITE; STRESS ACTIVATED PROTEIN KINASE; MITOGEN ACTIVATED PROTEIN KINASE KINASE 4; SODIUM SELENITE;

ANTINEOPLASTIC ACTIVITY; ANTIOXIDANT ACTIVITY; APOPTOSIS; CANCER CELL; CANCER PREVENTION; CELL STRAIN HEPG2; HUMAN; HUMAN CELL; MOLECULAR MECHANICS; NOTE; PROTEIN FUNCTION; PROTEIN PHOSPHORYLATION; BIOLOGICAL MODEL; CELL SURVIVAL; DIET SUPPLEMENTATION; DRUG EFFECT; GENE EXPRESSION REGULATION; METABOLISM; SIGNAL TRANSDUCTION; TUMOR CELL LINE;

APOPTOSIS; CELL LINE, TUMOR; CELL SURVIVAL; DIETARY SUPPLEMENTS; GENE EXPRESSION REGULATION, ENZYMOLOGIC; GENE EXPRESSION REGULATION, NEOPLASTIC; HUMANS; MAP KINASE KINASE 4; MAP KINASE SIGNALING SYSTEM; MODELS, BIOLOGICAL; REACTIVE OXYGEN SPECIES; SIGNAL TRANSDUCTION; SODIUM SELENITE;

EID: 45349092273     PISSN: 15384047     EISSN: 15558576     Source Type: Journal    
DOI: 10.4161/cbt.7.5.6088     Document Type: Note

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