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Activation of GSK3 Prevents Termination of TNF-Induced Signaling
Author(s) -
Bastian Welz,
Rolf Bikker,
Leonie Hoffmeister,
Mareike Diekmann,
Martin Christmann,
Korbinian Brand,
René Huber
Publication year - 2021
Publication title -
journal of inflammation research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.656
H-Index - 33
ISSN - 1178-7031
DOI - 10.2147/jir.s300806
Subject(s) - phosphorylation , gene knockdown , protein kinase c , signal transduction , small interfering rna , tumor necrosis factor alpha , biology , kinase , microbiology and biotechnology , proinflammatory cytokine , inflammation , immunology , transfection , biochemistry , apoptosis , gene
Termination of TNF-induced signaling plays a key role in the resolution of inflammation with dysregulations leading to severe pathophysiological conditions (sepsis, chronic inflammatory disease, cancer). Since a recent phospho-proteome analysis in human monocytes suggested GSK3 as a relevant kinase during signal termination, we aimed at further elucidating its role in this context.

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