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MicroRNAs modulate the noncanonical transcription factor NF-kappaB pathway by regulating expression of the kinase IKKalpha during macrophage differentiation.

Authors
Li, T; Morgan, MJ; Choksi, S; Zhang, Y; Kim, YS; Liu, ZG
Citation
Nature immunology, 11(9):799-805, 2010
Journal Title
Nature immunology
ISSN
1529-29081529-2916
Abstract
MicroRNAs are key regulators of many biological processes, including cell differentiation. Here we show that during human monocyte-macrophage differentiation, expression of the microRNAs miR-223, miR-15a and miR-16 decreased considerably, which led to higher expression of the serine-threonine kinase IKKalpha in macrophages. In macrophages, higher IKKalpha expression in conjunction with stabilization of the kinase NIK induced larger amounts of p52. Because of low expression of the transcription factor RelB in untreated macrophages, high p52 expression repressed basal transcription of both canonical and noncanonical NF-kappaB target genes. However, proinflammatory stimuli in macrophages resulted in greater induction of noncanonical NF-kappaB target genes. Thus, a decrease in certain microRNAs probably prevents macrophage hyperactivation yet primes the macrophage for certain responses to proinflammatory stimuli.
MeSH terms
Cell Differentiation/*immunologyCells, Cultured*Gene Expression Regulation, DevelopmentalGene Knockdown TechniquesHela CellsHumansI-kappa B Kinase/*immunology/*metabolismMacrophages/cytology/*immunologyMicroRNAs/*immunologyNF-kappa B/genetics/*immunologySignal TransductionU937 CellsUp-Regulation
DOI
10.1038/ni.1918
PMID
20711193
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Biochemistry & Molecular Biology
AJOU Authors
김, 유선
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