Overexpression of Aurora A by loss of CHFR gene expression increases the growth and survival of HTLV-1-infected T cells through enhanced NF-κB activity

International Journal of Cancer

Volumn 124, Issue 11, 2009, Pages 2607-2615

  Tomita, Mariko ^a   Toyota, Minoru ^b   Ishikawa, Chie ^a   Nakazato, Tetsuro ^a   Okudaira, Taeko ^a   Matsuda, Takehiro ^a   Uchihara, Jun Nosuke ^c   Taira, Naoya ^d   Ohshiro, Kazuiku ^e   Senba, Masachika ^f   Tanaka, Yuetsu ^a   Ohshima, Koichi ^g   Saya, Hideyuki ^h   Tokino, Takashi ^b   Mori, Naoki ^a  

^a UNIVERSITY OF THE RYUKYUS   (Japan)

^b SAPPORO MEDICAL UNIVERSITY   (Japan)

^c Naha City Hospital   (Japan)

^d Heartlife Hospital   (Japan)

^e Children's Medical Center   (Japan)

^f NAGASAKI UNIVERSITY   (Japan)

^g KURUME UNIVERSITY SCHOOL OF MEDICINE   (Japan)

^h KEIO UNIVERSITY SCHOOL OF MEDICINE   (Japan)

Author keywords

ATL; Aurora A; Aurora kinase inhibitor; CHFR; HTLV 1

Indexed keywords

AURORA A KINASE; AURORA KINASE INHIBITOR; IMMUNOGLOBULIN ENHANCER BINDING PROTEIN; MESSENGER RNA; RING FINGER PROTEIN; SURVIVIN; AURKA PROTEIN, HUMAN; CELL CYCLE PROTEIN; CHFR PROTEIN, HUMAN; PROTEIN SERINE THREONINE KINASE; TUMOR PROTEIN;

ADULT; ARTICLE; BIOLOGICAL ACTIVITY; CELL GROWTH; CELL LINE; CELL SURVIVAL; CONTROLLED STUDY; ENZYME PHOSPHORYLATION; GENE LOSS; GENE OVEREXPRESSION; GENETIC TRANSFECTION; HUMAN; HUMAN CELL; HUMAN T CELL LEUKEMIA VIRUS 1; HUMAN TISSUE; METHYLATION; ONCOGENE; PLASMID; PRIORITY JOURNAL; PROMOTER REGION; PROTEIN EXPRESSION; REPORTER GENE; T CELL LEUKEMIA; T LYMPHOCYTE; APOPTOSIS; CELL CYCLE; CELL PROLIFERATION; DNA METHYLATION; DRUG ANTAGONISM; ENZYMOLOGY; GENETICS; METABOLISM; PATHOLOGY; PHYSIOLOGY; SIGNAL TRANSDUCTION; VIROLOGY;

APOPTOSIS; CELL CYCLE; CELL CYCLE PROTEINS; CELL LINE; CELL PROLIFERATION; CELL SURVIVAL; DNA METHYLATION; HUMAN T-LYMPHOTROPIC VIRUS 1; HUMANS; LEUKEMIA-LYMPHOMA, ADULT T-CELL; NEOPLASM PROTEINS; NF-KAPPA B; PROTEIN-SERINE-THREONINE KINASES; SIGNAL TRANSDUCTION; T-LYMPHOCYTES;

EID: 64249134805     PISSN: 00207136     EISSN: 10970215     Source Type: Journal    
DOI: 10.1002/ijc.24257     Document Type: Article

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