Defective binding of IRFs to the initiator element of interleukin-1β-converting enzyme (ICE) promoter in an interferon-resistant Daudi subline

被引:16
作者
Iwase, S
Furukawa, Y
Kikuchi, J
Saito, S
Nakamura, M
Nakayama, R
Horiguchi-Yamada, J
Yamada, H
机构
[1] Jikei Univ, Sch Med, Dept Internal Med Aoto, Tokyo 1258506, Japan
[2] Jichi Med Sch, Ctr Mol Med, Div Mol Hemopoiesis, Minamimaki, Tochigi 3290498, Japan
[3] Jichi Med Sch, Dept Hematol, Minamimaki, Tochigi 3290498, Japan
[4] Hitachi Koki Co Ltd, Katsuta Res Lab, Katsuta, Ibaraki 312, Japan
[5] Jikei Univ, Sch Med, Inst DNA Med, Dept Oncol, Tokyo 105, Japan
[6] Jikei Univ, Sch Med, Inst DNA Med, Dept Genet, Tokyo 105, Japan
来源
FEBS LETTERS | 1999年 / 450卷 / 03期
关键词
interferon; drug resistance; IRF; ICE; initiator; promoter;
D O I
10.1016/S0014-5793(99)00515-3
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
To investigate mechanisms of interferon (IFN) resistance, we have established an IFN-resistant Daudi subline (Daudi(res)), which is 1x10(4) times more resistant to IFN-alpha than parental cells, Among the IFN-inducible genes examined, only ICE mRNA expression was deficient in Daudi(res) cells. We then analyzed the regulatory mechanisms of ICE transcription, and found that IFN-induced activation of the ICE promoter was dependent on the binding of IRFs to its initiator (Inr) element. Inr binding of IRFs was markedly diminished in Daudi(res) cells, and forced expression of IRF-1 was able to activate the ICE promoter to the level of parental cells. These results suggest that IRFs and their target genes, as represented by ICE in this study, are involved in IFN resistance, (C) 1999 Federation of European Biochemical Societies.
引用
收藏
页码:263 / 267
页数:5
相关论文
共 24 条
[1]   STRUCTURE OF 2 FORMS OF THE INTERFERON-INDUCED (2-'-5-') OLIGO-A SYNTHETASE OF HUMAN-CELLS BASED ON CDNAS AND GENE-SEQUENCES [J].
BENECH, P ;
MORY, Y ;
REVEL, M ;
CHEBATH, J .
EMBO JOURNAL, 1985, 4 (09) :2249-2256
[2]   MOLECULAR CHARACTERIZATION OF THE GENE FOR HUMAN INTERLEUKIN-1-BETA CONVERTING-ENZYME (IL1BC) [J].
CERRETTI, DP ;
HOLLINGSWORTH, LT ;
KOZLOSKY, CJ ;
VALENTINE, MB ;
SHAPIRO, DN ;
MORRIS, SW ;
NELSON, N .
GENOMICS, 1994, 20 (03) :468-473
[3]   JAK-STAT PATHWAYS AND TRANSCRIPTIONAL ACTIVATION IN RESPONSE TO IFNS AND OTHER EXTRACELLULAR SIGNALING PROTEINS [J].
DARNELL, JE ;
KERR, IM ;
STARK, GR .
SCIENCE, 1994, 264 (5164) :1415-1421
[4]   HUMAN TRANSCRIPTION FACTOR USF STIMULATES TRANSCRIPTION THROUGH THE INITIATOR ELEMENTS OF THE HIV-1 AND THE AD-ML PROMOTERS [J].
DU, H ;
ROY, AL ;
ROEDER, RG .
EMBO JOURNAL, 1993, 12 (02) :501-511
[5]   CYTOKINE THERAPEUTICS - LESSONS FROM INTERFERON-ALPHA [J].
GUTTERMAN, JU .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (04) :1198-1205
[6]   STRUCTURALLY SIMILAR BUT FUNCTIONALLY DISTINCT FACTORS, IRF-1 AND IRF-2, BIND TO THE SAME REGULATORY ELEMENTS OF IFN AND IFN-INDUCIBLE GENES [J].
HARADA, H ;
FUJITA, T ;
MIYAMOTO, M ;
KIMURA, Y ;
MARUYAMA, M ;
FURIA, A ;
MIYATA, T ;
TANIGUCHI, T .
CELL, 1989, 58 (04) :729-739
[7]   Modulation of E2F activity is linked to interferon-induced growth suppression of hematopoietic cells [J].
Iwase, S ;
Furukawa, Y ;
Kikuchi, J ;
Nagai, M ;
Terui, Y ;
Nakamura, M ;
Yamada, H .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (19) :12406-12414
[8]   CELLS RESISTANT TO INTERFERON ARE DEFECTIVE IN ACTIVATION OF A PROMOTER-BINDING FACTOR [J].
KESSLER, DS ;
PINE, R ;
PFEFFER, LM ;
LEVY, DE ;
DARNELL, JE .
EMBO JOURNAL, 1988, 7 (12) :3779-3783
[9]   A GENERAL-METHOD FOR RAPID SITE-DIRECTED MUTAGENESIS USING THE POLYMERASE CHAIN-REACTION [J].
LANDT, O ;
GRUNERT, HP ;
HAHN, U .
GENE, 1990, 96 (01) :125-128
[10]   MOLECULAR-CLONING AND CHARACTERIZATION OF THE HUMAN DOUBLE-STRANDED-RNA ACTIVATED PROTEIN-KINASE INDUCED BY INTERFERON [J].
MEURS, E ;
CHONG, K ;
GALABRU, J ;
THOMAS, NSB ;
KERR, IM ;
WILLIAMS, BRG ;
HOVANESSIAN, AG .
CELL, 1990, 62 (02) :379-390