期刊
NATURE IMMUNOLOGY
卷 7, 期 4, 页码 375-381出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni1308
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- NIAID NIH HHS [AI30165] Funding Source: Medline
- NIGMS NIH HHS [GM61710] Funding Source: Medline
The MyD88 adaptor protein is critical in Toll-like receptor and interleukin 1 receptor (IL-1R) signaling, but has not been linked to interferon-gamma receptor (IFN-gamma R) signaling. Here we demonstrate that MyD88 increased the half-life but not the synthesis of IFN-gamma-induced mRNA transcripts encoding tumor necrosis factor and IFN-gamma-inducible protein 10. IFN-gamma stimulation triggered a physical association between the IFN-gamma R1 and MyD88. Transcript stabilization required activation of mixed-lineage kinase 3 and p38 mitogen-activated protein kinase and the presence of an adenine-uridine-rich element in the transcript's 3' untranslated region. These results demonstrate a MyD88-dependent post-transcriptional mechanism through which IFN-gamma can enhance the expression of genes encoding proinflammatory molecules.
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