GATA‐3 represses gp91phox gene expression in eosinophil‐committed HL‐60‐C15 cells

FEBS Letters

Anowar Sadat, Mohammed³  Nakamura, Michio¹  Tsuji, Yoshiro³  Kumatori, Atsushi¹  Yamaguchi, Yuji²  Suzuki, Shoichi¹ 

[1] Department of Biochemistry, Institute of Tropical Medicine, Nagasaki University, Nagasaki 852, Japan;Department of Cell Differentiation, Institute of Molecular Embryology and Genetics, Kumamoto University School of Medicine, Kumamoto, Japan;Department of Pediatrics, Nagasaki University School of Medicine, 1-7-1, Sakamoto, Nagasaki 852, Japan

关键词: gp91phox;    Eosinophil;    Chronic granulomatous disease;    GATA-3;    GATA consensus site;    CGD;    chronic granulomatous disease;    BID;    binding increased during differentiation;    INF-γ;    interferon-γ;    CDP;    CCAAT displacement protein;    IRF;    interferon responsive factor;    EMSA;    electrophoretic mobility shift assay;    TBP;    TATA box binding protein;    TCRβ;    T-cell receptor β;   

DOI  :  10.1016/S0014-5793(98)01182-X

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

To study the regulatory mechanism of gp91^phox gene expression in eosinophils, we transiently transfected eosinophil-committed HL-60-C15 cells with gp91^phox promoter constructs, and identified a negative element from bp −267 to −246 of the gp91^phox gene, the deletion of which caused an 83% increase in promoter activity. Electrophoresis mobility shift assays demonstrated GATA-3 binds to the GATA consensus site from bp −256 to −250. An 81% increment in promoter activity was obtained when a mutation was introduced in the GATA-3 binding site of the bp −267 to +12 construct, which is comparable to that of the bp −245 to +12 construct. We therefore conclude that GATA-3 specifically binding to the GATA site negatively regulates the expression of the gene in HL-60-C15 cells.

【 授权许可】

Unknown