Ube1L and protein ISGylation are not essential for alpha/beta interferon signaling
| Autor: | Juan Carlos de la Torre, Keun Il Kim, Oxana A. Malakhova, Jiann-Kae Luo, Mei-Feng Shen, Weiguo Zou, Ming Yan, Dong-Er Zhang |
|---|---|
| Rok vydání: | 2005 |
| Předmět: |
Alpha (ethology)
Apoptosis Ubiquitin-Activating Enzymes Biology stat Vesicular stomatitis Indiana virus Mice Interferon Rhabdoviridae Infections Endopeptidases medicine Animals Arenaviridae Infections Lymphocytic choriomeningitis virus Beta (finance) Molecular Biology Ubiquitins Cells Cultured chemistry.chemical_classification Mice Knockout Innate immune system Interferon-alpha Cell Biology Interferon-beta Articles biology.organism_classification ISG15 Virology Cell biology Enzyme chemistry Vesicular stomatitis virus Mutation Cytokines Ubiquitin Thiolesterase medicine.drug Signal Transduction |
| Zdroj: | Molecular and cellular biology. 26(2) |
| ISSN: | 0270-7306 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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