期刊
JOURNAL OF GENERAL VIROLOGY
卷 89, 期 -, 页码 1881-1889出版社
SOC GENERAL MICROBIOLOGY
DOI: 10.1099/vir.0.83643-0
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资金
- Biotechnology and Biological Sciences Research Council [BBS/E/I/00001258] Funding Source: researchfish
- Biotechnology and Biological Sciences Research Council [BBS/E/I/00001258] Funding Source: Medline
- BBSRC [BBS/E/I/00001258] Funding Source: UKRI
Classical swine fever virus (CSFV) belongs to the genus Pestivirus and is the causative agent of classical swine fever, a haemorrhagic disease of pigs. The virus replicates in host cells without activating interferon (IFN) production and has been reported to be an antagonist of doublestranded RNA-induced apoptosis. The N-terminal protease (N pro) of CSFV is responsible for this evasion of the host innate immune response. In order to identify cellular proteins that interact with the N pro product of CSFV, a yeast two-hybrid screen of a human library was carried out, which identified li Bj,, the inhibitor of NF-i 13, a transcription factor involved in the control of apoptosis, the immune response and IFN production. The IN pro_, i 13),. interaction was confirmed using yeast two-hybrid analysis and additional co-precipitation assays. It was also shown that N pro localizes to both the cytoplasmic and nuclear compartments in stably transfected cells and in CSFVinfected cells. Following stimulation by tumour necrosis factor alpha, PK-1 5 cell lines expressing Nor' exhibited transient nuclear accumulation of pli,713j., but no effect of CSFV infection on li B:t. localization or Nl`-/ B p65 activation was observed.
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