ERK1/2 activation plays important roles in the opposite effects of Trichostatin A in non-cancer and cancer cells

Toxicon

Volumn 57, Issue 6, 2011, Pages 932-937

  Zhang, Yong ^a,b   Yu, Guoyu ^a,c   Wang, Dongmei ^d   Hu, Ying ^d   Lei, Weiwei ^a,d  

^a KUNMING UNIVERSITY OF SCIENCE AND TECHNOLOGY   (China)

^b KUNMING INSTITUTE OF ZOOLOGY   (China)

^c KUNMING MEDICAL UNIVERSITY   (China)

^d INSTITUTE OF BIOCHEMISTRY AND CELL BIOLOGY   (China)

Author keywords

Apoptosis; Cancer cells; ERK1 2; HDAC inhibitor; Non cancer cells; TSA

Indexed keywords

HISTONE DEACETYLASE INHIBITOR; MITOGEN ACTIVATED PROTEIN KINASE 1; MITOGEN ACTIVATED PROTEIN KINASE 3; TRANSFORMING GROWTH FACTOR BETA1; TRICHOSTATIN A;

ANIMAL CELL; APOPTOSIS; ARTICLE; CANCER CELL CULTURE; CONTROLLED STUDY; DRUG CYTOTOXICITY; DRUG MECHANISM; ENZYME ACTIVATION; ENZYME PHOSPHORYLATION; FEMALE; HUMAN; HUMAN CELL; NONHUMAN; PRIORITY JOURNAL; PROTEIN FUNCTION; STARVATION; STREPTOMYCES;

3T3-L1 CELLS; ANIMALS; APOPTOSIS; CELL LINE, TUMOR; DOGS; ENZYME ACTIVATION; FLOW CYTOMETRY; HISTONE DEACETYLASE INHIBITORS; HUMANS; HYDROXAMIC ACIDS; IMMUNOBLOTTING; MICE; MITOGEN-ACTIVATED PROTEIN KINASE 3; TRANSFORMING GROWTH FACTOR BETA1;

STREPTOMYCES;

EID: 79955006018     PISSN: 00410101     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.toxicon.2011.03.008     Document Type: Article

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