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S100A9 activates ERK. 13 / 13
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"Furthermore, treatment with RAGE blocking antibodies also abrogated the S100A9-induced p38 and ERK1/2 activation, suggesting that S100A9-induced MAPK activation is mediated via RAGE ligation."
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"In this study, we illustrated that IL-37b could suppress transcriptional levels of PYCARD, S100A9, and CAMP genes, and antagonize the activation of NF-kappaB, PI3K-Akt, and ERK1/2 pathways in eosinophils, which elucidate the intracellular signaling cascade to suppress the bacterial TLR2 mediated activation in eosinophils upon interaction with human bronchial epithelial cells, and ameliorate the exacerbated allergic airway inflammation in HDM humanized asthmatic mice."
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"When phosphorylation of p38 and Erk1/2 was compared, no significant changes in P-p38 were obvious (not shown); S100A9 and S100A8/A9 pretreatments increased p-Erk1/2 above amounts found in lungs from mice treated with LPS alone (XREF_FIG)."
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"Collectively, these data suggest that monocytes and macrophages in liver metastases induced tumor cell proliferation, migration and invasion, and upregulated S100a8 and S100a9 expression through TNFalpha induced ERK activation."
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"MP1 (MEK partner 1) is an ERK1/2 scaffold that is specifically targeted to endosomes by the adaptor protein P14."
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"DP, S100A8, and S100A9 activate Lyn, PI3K, Akt, ERK and NF-kappaB, and suppress caspase 9/3 pathway in normal and asthmatic neutrophils (Figs XREF_FIG, XREF_FIG and XREF_FIG)."
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"S100A9 triggers NF-kappaB responses in THP-1 cells (Riva et al., 2012), triggers NF-kappaB and ERK1/2 MAPK responses in lung cells (Xu et al., 2013), and induces IL-6, IL-8 secretion from PBMC via NF-[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"P14 knockdown inhibited efficient ERK signaling to p90RSK (ribosomal protein S6 kinase) in the cytoplasm and inhibited ERK signaling to an Elk1 luciferase reporter in a dose dependent manner, corresponding to the extent of p14 knockdown."
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"We therefore reasoned that RAGE could be the receptor responsible for enhanced activity of p38 and ERK1/2 MAPKs driven by S100A9 in HepG2 cells."
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"DP, S100A8, and S100A9 activate Lyn, PI3K, Akt, ERK and NF-κB, and suppress caspase 9/3 pathway in normal and asthmatic neutrophils (Figs xref , xref and xref )."
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"Preliminary experiments regarding the crosstalk between MAPKs and STAT3 signaling pathways are currently under investigation to clarify this detailed mechanism of the in vivo mouse model as well as the in vitro cell culture system.In conclusion, we demonstrated that S100A9, one component of calprotectin, activates p38, ERK, and STAT3 signaling pathways, resulting in increased IL-6 and RANKL expressions in mouse osteocyte-like cells."
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"Thus, S100A9 induced THP-1 cell migration requires MEK and ERK, NF-kappaB and PI3K activity, but not p38 MAPK."
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"These results are in agreement with a study of Xu et al., which showed that S100A9, a ligand of RAGE, activated ERK signaling in order to drive collagen III transcriptional expression [XREF_BIBR]."
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