Lack of c-jun activity increases survival to cisplatin

FEBS Letters

Volumn 453, Issue 1-2, 1999, Pages 151-158

  Sánchez Pérez, Isabel ^a   Perona, Rosario ^a  

^a CSIC   (Spain)

Author keywords

Apoptosis; Cisplatin; CPP32; DNA damage; JNK1; Jun

Indexed keywords

CASPASE 3; CISPLATIN; DOXORUBICIN; STRESS ACTIVATED PROTEIN KINASE; SYNAPTOPHYSIN; TRANSCRIPTION FACTOR AP 1;

ANTINEOPLASTIC ACTIVITY; APOPTOSIS; ARTICLE; CELL DEATH; CELL SURVIVAL; CELL VIABILITY; CONTROLLED STUDY; DNA DAMAGE; DRUG MECHANISM; ENZYME ACTIVATION; HUMAN; HUMAN CELL; KNOCKOUT MOUSE; PRIORITY JOURNAL;

ACTIVATING TRANSCRIPTION FACTOR 2; ANIMALS; ANTINEOPLASTIC AGENTS; APOPTOSIS; CA(2+)-CALMODULIN DEPENDENT PROTEIN KINASE; CASPASE 3; CASPASES; CELL SURVIVAL; CISPLATIN; CYCLIC AMP RESPONSE ELEMENT-BINDING PROTEIN; DOXORUBICIN; ENZYME ACTIVATION; JNK MITOGEN-ACTIVATED PROTEIN KINASES; MAP KINASE KINASE 4; MAP KINASE KINASE KINASE 1; MICE; MICE, KNOCKOUT; MITOGEN-ACTIVATED PROTEIN KINASE KINASES; MITOGEN-ACTIVATED PROTEIN KINASES; PROTEIN KINASES; PROTEIN-SERINE-THREONINE KINASES; PROTO-ONCOGENE PROTEINS C-FOS; PROTO-ONCOGENE PROTEINS C-JUN; SIGNAL TRANSDUCTION; TRANSCRIPTION FACTOR AP-1; TRANSCRIPTION FACTORS;

EID: 0344258124     PISSN: 00145793     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0014-5793(99)00690-0     Document Type: Article

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