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Dev Comp Immunol ; 57: 48-56, 2016 Apr.
Article in English | MEDLINE | ID: mdl-26719025

ABSTRACT

The BTB-POZ transcription factor Promyelocytic Leukemia Zinc Finger (PLZF, or ZBTB16) has been recently identified as a major factor regulating the induction of a subset of Interferon stimulated genes in human and mouse. We show that the two co-orthologues of PLZF found in zebrafish show distinct expression patterns, especially in larvae. Although zbtb16a/plzfa and zbtb16b/plzfb are not modulated by IFN produced during viral infection, their over-expression increases the level of the early type I IFN response, at a critical phase in the race between the virus and the host response. The effect of Plzfb on IFN induction was also detectable after cell infection by different non-enveloped RNA viruses, but not after infection by the rhabdovirus SVCV. Our findings indicate that plzf implication in the regulation of type I IFN responses is conserved across vertebrates, but at multiple levels of the pathway and through different mechanisms.


Subject(s)
Interferon Type I/immunology , Kruppel-Like Transcription Factors/metabolism , RNA Virus Infections/immunology , RNA Viruses/immunology , Zebrafish Proteins/metabolism , Zebrafish/immunology , Animals , Humans , Immunity, Innate , Interferon Type I/metabolism , Kruppel-Like Transcription Factors/classification , Kruppel-Like Transcription Factors/genetics , Mice , Phylogeny , Poly I-C/immunology , Promyelocytic Leukemia Zinc Finger Protein , RNA, Viral/immunology , Transcriptome , Zebrafish/genetics , Zebrafish Proteins/classification , Zebrafish Proteins/genetics
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