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J. Simon C. Arthur

Researcher at University of Dundee

Publications -  142
Citations -  15322

J. Simon C. Arthur is an academic researcher from University of Dundee. The author has contributed to research in topics: Kinase & CREB. The author has an hindex of 56, co-authored 129 publications receiving 13768 citations. Previous affiliations of J. Simon C. Arthur include Queen's University & Medical Research Council.

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The selectivity of protein kinase inhibitors: a further update.

TL;DR: Harmine has been identified as a potent and specific inhibitor of DYRK1A (dual-specificity tyrosine-phosphorylated and -regulated kinase 1A) in vitro and the results have further emphasized the need for considerable caution in using small-molecule inhibitors of protein kinases to assess the physiological roles of these enzymes.
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Mitogen-activated protein kinases in innate immunity

TL;DR: This Review discusses the current knowledge about the regulation and the function of MAPKs in innate immunity, as well as the importance of negative feedback loops in limiting MAPK activity to prevent host tissue damage and how pathogens have evolved complex mechanisms to manipulate MAPK activation to increase their virulence.
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MSK2 and MSK1 mediate the mitogen‐ and stress‐induced phosphorylation of histone H3 and HMG‐14

TL;DR: It is concluded that MSKs are the major kinases for histone H3 and HMG‐14 in response to mitogenic and stress stimuli in fibroblasts.
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The role of 3-phosphoinositide-dependent protein kinase 1 in activating AGC kinases defined in embryonic stem cells.

TL;DR: PDK1 mediates activation of PKB, p70 S6 kinase and p90 Rsk in vivo, but is not rate-limiting foractivation of PKA, MSK1 and AMPK.
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MSK1 and MSK2 are required for the mitogen- and stress-induced phosphorylation of CREB and ATF1 in fibroblasts.

TL;DR: It is shown that MSK1 and MSK2 are required for the stress-induced phosphorylation of transcription factors CREB and ATF1 in primary embryonic fibroblasts, which results in a 50% reduction in c-fos and junB gene transcription in response to anisomycin or UV-C radiation.