Abstract
ARE-mRNAs are actively degraded with tristetraprolin (TTP) in resting cells while they turn into stable messengers in activated cells. P38 plays a crucial role in stabilizing ARE-mRNA. Here we reveal that P38 activation represses the interaction between TTP and Ago2, thus restraining TTP from being targeted into processing bodies and stabilizing ARE-mRNA.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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3' Untranslated Regions
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AU Rich Elements*
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Argonaute Proteins / genetics
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Argonaute Proteins / metabolism*
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Gene Expression Regulation
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HEK293 Cells
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HeLa Cells
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Humans
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Lipopolysaccharides / pharmacology
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Phosphorylation
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RNA Stability*
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RNA, Messenger / genetics*
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Transcription, Genetic / drug effects
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Tristetraprolin / genetics
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Tristetraprolin / metabolism*
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Tumor Necrosis Factor-alpha / genetics
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Tumor Necrosis Factor-alpha / metabolism
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p38 Mitogen-Activated Protein Kinases / metabolism*
Substances
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3' Untranslated Regions
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AGO2 protein, human
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Argonaute Proteins
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Lipopolysaccharides
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RNA, Messenger
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Tristetraprolin
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Tumor Necrosis Factor-alpha
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p38 Mitogen-Activated Protein Kinases