Journal
MOLECULAR AND CELLULAR BIOLOGY
Volume 26, Issue 2, Pages 472-479Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.26.2.472-479.2006
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Funding
- NATIONAL CANCER INSTITUTE [R01CA079849] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM066955] Funding Source: NIH RePORTER
- NCI NIH HHS [R01 CA079849, CA079849] Funding Source: Medline
- NIGMS NIH HHS [R01 GM066955, GM066955] Funding Source: Medline
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The expression of ubiquitin-like modifier ISG15 and its conjugation to target proteins are highly induced by interferon (IFN) stimulation and during viral and bacterial infections. However, the biological significance of this modification has not been clearly understood. To investigate the function of protein modification by ISG15, we generated a mouse model deficient in UBE1L, an ISG15-activating enzyme. Ube1L(-/-) mice did not produce ISG15 conjugates but expressed free ISG15 normally. ISGylation has been implicated in the reproduction and innate immunity. However, Ube1L(-/-) mice were fertile and exhibited normal antiviral responses against vesicular stomatitis virus and lymphocytic choriomeningitis virus infection. Our results indicate that UBE1L and protein ISGylation are not critical for IFN-alpha/beta signaling via JAK/STAT activation. Moreover, using Ube1L/Ubp43 double-deficient mice, we showed that lack of UBP43, but not the increase of protein ISGylation, is related to the increased IFN signaling in Ubp43-deficient mice.
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