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J Biol Chem, Vol. 275, Issue 12, 8880-8888, March 24, 2000
From the The 2-5A system is an interferon-regulated RNA
degradation pathway with antiviral, growth-inhibitory, and
pro-apoptotic activities. RNase-L mediates the antiviral activity
through the degradation of viral RNAs, and the anticellular effects of
the 2-5A system are thought to be similarly mediated through the
degradation of cellular transcripts. However, specific
RNase-L-regulated cellular RNAs have not been identified. To isolate
candidate RNase-L substrates, differential display was used to identify
mRNAs that exhibited increased expression in RNase-L-deficient
N1E-115 cells as compared with RNase-L-transfected cells. A novel
interferon-stimulated gene encoding a 43-kDa ubiquitin-specific
protease, designated ISG43, was identified in this screen. ISG43
expression is induced by interferon and negatively regulated by
RNase-L. ISG43 induction is a primary response to interferon treatment
and requires a functional JAK/STAT signaling pathway. The kinetics of
ISG43 induction were identical in wild type and RNase-L knock-out
fibroblasts; however, the decline in ISG43 mRNA following
interferon treatment was markedly attenuated in RNase-L knock-out
fibroblasts. The delayed shut-off kinetics of ISG43 mRNA
corresponded to an increase in its half-life in RNase-L-deficient
cells. ISG15 mRNA also displayed RNase-L-dependent regulation. These findings identify a novel role for the 2-5A system
in the attenuation of the interferon response.
The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EMBL Data Bank with accession number(s) AF176642.
RNase-L-dependent Destabilization of Interferon-induced
mRNAs
A ROLE FOR THE 2-5A SYSTEM IN ATTENUATION OF THE INTERFERON
RESPONSE*
,§,,¶
, and¶**
Greenebaum Cancer Center, Program in
Oncology, Department of Microbiology and Immunology, and
¶ Molecular and Cell Biology Program, University of Maryland,
Baltimore, Maryland 21201
*
This work was supported by NIAID Grant AI39608 from the
National Institutes of Health (to B. A. H.) and by Grants CA71401 and
CA78282 from the National Institutes of Health (to D. K.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
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