Interfering with cellular signaling pathways enhances sensitization to combined sodium butyrate and GCV treatment in EBV-positive tumor cells

Virus Research

Volumn 135, Issue 1, 2008, Pages 175-180

  He, Yuwen ^a   Cai, Shaohui ^b   Zhang, Ge ^a   Li, Xiaoqing ^a   Pan, Liting ^a   Du, Jun ^a  

^a SUN YAT SEN UNIVERSITY   (China)

^b JINAN UNIVERSITY   (China)

Author keywords

Akt; Epstein Barr virus; Ganciclovir; MEKK1; Sodium butyrate; Thymidine kinase

Indexed keywords

BUTYRIC ACID; GANCICLOVIR; MITOGEN ACTIVATED PROTEIN KINASE KINASE KINASE 1; PROTEIN KINASE B; RAF PROTEIN; RAS PROTEIN; THYMIDINE KINASE;

ARTICLE; CELL VIABILITY; CONTROLLED STUDY; CYTOTOXICITY; DRUG INHIBITION; ENZYME ACTIVATION; ENZYME ACTIVITY; EPSTEIN BARR VIRUS; IMMUNOBLOTTING; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; SENSITIZATION; TUMOR CELL;

BUTYRATES; CELL LINE, TUMOR; CELL SURVIVAL; DRUG THERAPY, COMBINATION; EPSTEIN-BARR VIRUS INFECTIONS; GANCICLOVIR; GENE EXPRESSION REGULATION, NEOPLASTIC; HERPESVIRUS 4, HUMAN; HUMANS; MAP KINASE KINASE KINASE 1; NEOPLASMS; ONCOGENE PROTEIN P21(RAS); ONCOGENE PROTEIN V-AKT; RAF KINASES; SIGNAL TRANSDUCTION; THYMIDINE KINASE;

HUMAN HERPESVIRUS 4;

EID: 44549086934     PISSN: 01681702     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.virusres.2008.03.012     Document Type: Article

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