Post-transcriptional control of the interferon system

被引:66
作者
Khabar, Khalid S. A.
Young, Howard A.
机构
[1] King Faisal Specialist Hosp & Res Ctr, Program BioMol Res, Riyadh 11211, Saudi Arabia
[2] Natl Canc Inst, Canc Res Ctr, Expt Immunol Lab, Ft Detrick, MD 21702 USA
关键词
interferons; post-transcriptional; 3 ' untranslated regions; mRNA stability; AU-rich elements;
D O I
10.1016/j.biochi.2007.02.008
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
The interferon (IFN) system is a well-controlled network of signaling, transcriptional, and post-transcriptional processes that orchestrate host defense against microbes. The IFN response comprises a multi-array of IFN-stimulated gene products that mediate a variety of biological processes designed to control infection and regulate specific immune responses. In this review, we focus on post-transcriptional mechanisms of gene regulation that occur during the course of IFN induction and during the response of cells to IFN. Post-transcriptional mechanisms involve different levels of regulation such as mRNA stability, alternative splicing, and translation. Such controls offer a fine tuning mechanism for efficient and rapid response and as a negative feedback control in IFN biosynthesis and response. (C) 2007 Elsevier Masson SAS. All rights reserved.
引用
收藏
页码:761 / 769
页数:9
相关论文
共 88 条
[1]   TYPE-I INTERFERONS (IFN-ALPHA AND IFN-BETA) SUPPRESS CYTOTOXIN (TUMOR-NECROSIS-FACTOR-ALPHA AND LYMPHOTOXIN)PRODUCTION BY MITOGEN-STIMULATED HUMAN PERIPHERAL-BLOOD MONONUCLEAR-CELLS [J].
ABUKHABAR, KS ;
ARMSTRONG, JA ;
HO, M .
JOURNAL OF LEUKOCYTE BIOLOGY, 1992, 52 (02) :165-172
[2]  
Anderson P, 2002, CELL STRESS CHAPERON, V7, P213, DOI 10.1379/1466-1268(2002)007<0213:VSTROE>2.0.CO
[3]  
2
[4]   ARED: human AU-rich element-containing mRNA database reveals an unexpectedly diverse functional repertoire of encoded proteins [J].
Bakheet, T ;
Frevel, M ;
Williams, BRG ;
Greer, W ;
Khabar, KSA .
NUCLEIC ACIDS RESEARCH, 2001, 29 (01) :246-254
[5]   ARED 3.0: the large and diverse AU-rich transcriptome [J].
Bakheet, Tala ;
Williams, Bryan R. G. ;
Khabar, Khalid S. A. .
NUCLEIC ACIDS RESEARCH, 2006, 34 :D111-D114
[6]   Essential role for the dsRNA-dependent protein kinase PKR in innate immunity to viral infection [J].
Balachandran, S ;
Roberts, PC ;
Brown, LE ;
Truong, H ;
Pattnaik, AK ;
Archer, DR ;
Barber, GN .
IMMUNITY, 2000, 13 (01) :129-141
[7]   AU-rich elements and associated factors: are there unifying principles? [J].
Barreau, C ;
Paillard, L ;
Osborne, HB .
NUCLEIC ACIDS RESEARCH, 2005, 33 (22) :7138-7150
[8]   Human interferon-γ mRNA autoregulates its translation through a pseudoknot that activates the interferon-inducible protein kinase PKR [J].
Ben-Asouli, Y ;
Banai, Y ;
Pel-Or, Y ;
Shir, A ;
Kaempfer, R .
CELL, 2002, 108 (02) :221-232
[9]   The 2′-5′ oligoadenylate/RNase L/RNase L inhibitor pathway regulates both MyoD mRNA stability and muscle cell differentiation [J].
Bisbal, C ;
Silhol, M ;
Laubenthal, K ;
Kaluza, T ;
Carnac, G ;
Milligan, L ;
Le Roy, F ;
Salehzada, T .
MOLECULAR AND CELLULAR BIOLOGY, 2000, 20 (14) :4959-4969
[10]   HERPES-SIMPLEX VIRUS TRANSREGULATORY PROTEIN ICP27 STABILIZES AND BINDS TO 3'-ENDS OF LABILE MESSENGER-RNA [J].
BROWN, CR ;
NAKAMURA, MS ;
MOSCA, JD ;
HAYWARD, GS ;
STRAUS, SE ;
PERERA, LP .
JOURNAL OF VIROLOGY, 1995, 69 (11) :7187-7195