ICBP90 Expression Is Downregulated in Apoptosis-Induced Jurkat Cells

Annals of the New York Academy of Sciences

Volumn 1010, Issue , 2003, Pages 300-303

  Abbady, Abdul Qader ^a   Bronner, Christian ^a   Trotzier, Marie Aline ^a   Hopfner, Raphael ^a   Bathami, Kawtar ^a   Muller, Christian D ^b   Jeanblanc, Michael ^a   Mousli, Marc ^a  

^a INSERM   (France)

^b CNRS   (France)

Author keywords

Apoptosis; Calcium; Cancer; Cell proliferation; ICBP90; Jurkat cells

Indexed keywords

BINDING PROTEIN; CALCIMYCIN; INVERTED CCAAT BOX BINDING PROTEIN 90; PHYTOHEMAGGLUTININ; UNCLASSIFIED DRUG;

APOPTOSIS; CANCER CELL; CARCINOGENESIS; CELL STIMULATION; CONCENTRATION RESPONSE; CONFERENCE PAPER; CONTROLLED STUDY; DOWN REGULATION; GENE EXPRESSION; HUMAN; HUMAN CELL; LEUKEMIA CELL LINE; PROTEIN EXPRESSION;

EID: 1342284282     PISSN: 00778923     EISSN: None     Source Type: Book Series    
DOI: 10.1196/annals.1299.052     Document Type: Conference Paper

References (5)

1. KAUFMANN, S.H. & G.J. GORES. 2000. Apoptosis in cancer: cause and cure. Bioessays 22: 1007-1017.
2. HOPFNER, R., M. MOUSLI, J.M. JELTSCH, et al. 2000. ICBP90, a novel human CCAAT binding protein, involved in the regulation of topoisomerase IIα expression. Cancer Res. 60: 121-128.
3. MOUSLI, M., R. HOPFNER, A.Q. ABBADY, et al. 2003. ICBP90 belongs to a new family of proteins with an expression that is deregulated in cancer cells. Br. J. Cancer 89: 120-127.
4. HOPFNER, R., M. MOUSLI, P. OUDET & C. BRONNER. 2002. Overexpression of ICBP90, a novel CCAAT-binding protein, overcomes cell contact inhibition by forcing topoisomerase IIα expression. Anticancer Res. 22: 3165-3170.
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