期刊
VIRUSES-BASEL
卷 9, 期 1, 页码 -出版社
MDPI AG
DOI: 10.3390/v9010002
关键词
RNA decay; RNA-protein interactions; decapping; Xrn1; exosome; TRAMP; exonuclease; RNAse; intrinsic immunity; antiviral
类别
资金
- National Institute of Health [R01AI074951, U54AI057168, R01AI095500, T32AI007324]
- Burroughs Wellcome Investigators in the Pathogenesis of Infectious Disease Award
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI074951, T32AI007324, U54AI057168, R01AI095500] Funding Source: NIH RePORTER
The innate immune system has evolved a number of sensors that recognize viral RNA (vRNA) to restrict infection, yet the full spectrum of host-encoded RNA binding proteins that target these foreign RNAs is still unknown. The RNA decay machinery, which uses exonucleases to degrade aberrant RNAs largely from the 5' or 3' end, is increasingly recognized as playing an important role in antiviral defense. The 5' degradation pathway can directly target viral messenger RNA (mRNA) for degradation, as well as indirectly attenuate replication by limiting specific pools of endogenous RNAs. The 3' degradation machinery (RNA exosome) is emerging as a downstream effector of a diverse array of vRNA sensors. This review discusses our current understanding of the roles of the RNA decay machinery in controlling viral infection.
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