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CYLD inhibits ERK. 18 / 23
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"These studies provide insights into the molecular mechanisms underlying the tight regulation of inflammation via inhibition of ERK by CYLD and identified vinpocetine as a potential therapeutic agent for suppressing the inflammatory response in the pathogenesis of OM via upregulating negative regulator CYLD expression."
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"As shown in XREF_FIG, CYLD WT inhibited ERK phosphorylation, while CYLD knockdown, via siCYLD, markedly enhanced ERK activation by NTHi (XREF_FIG)."
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"In addition, it is also possible that CYLD may inhibit ERK activation and inflammation via up-regulation of MAPK phosphatase-1 (MKP-1)."
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"However, it remains unknown if CYLD also suppresses ERK activation induced by bacterial pathogens."
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"These studies provide insights into the molecular mechanisms underlying the tight regulation of inflammation via inhibition of ERK by CYLD and identified vinpocetine as a potential therapeutic agent for suppressing the inflammatory response in the pathogenesis of OM via upregulating negative regulator CYLD expression."
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"Future studies will focus on using DUB activity deficient CYLD mutant constructs to determine whether DUB activity is essential for the CYLD mediated suppression of ERK signaling pathway induced by bacterial pathogens."
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"Vinpocetine inhibited S. pneumoniae -induced inflammatory response via inhibition of mitogen-activated protein kinase (MAPK) extracellular signal-regulated kinase (ERK) by CYLD."
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"Taken together, the CYLD suppression of ERK dependent IL-8 via MKP-1 may bring novel insights into the tight regulation of inflammatory responses and also lead to innovative therapeutic strategies for controlling these responses by targeting key negative regulators of inflammation."
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"We thus asked whether CYLD inhibited ERK activation."
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"CYLD also enhances oxidative stress by inhibiting the activation of the extracellular signal regulated kinase (ERK), p38/AP -1 and c-Myc pathways, ensuring Nrf2 downregulation."
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"CYLD inhibits NTHi induced activation of ERK."
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"CYLD Impairs Production of Cytokines, ROS, and NO and Reduces Activation of NF-kappaB, ERK1/2, and p38MAPK in Lm Infected BMDM."
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"Thus, it is possible that ERK or its upstream molecules including MEK1/2, Raf and MEKK1 (64, 65) may be polyubiquitinated via K63, and CYLD may inhibit the activation of ERK by deubiquitinating ERK or its upstream molecules."
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"Here we provide clear evidence that CYLD inhibits NTHi induced activation of ERK (XREF_FIG), and we also demonstrate that CYLD controls IL-8 expression via specifically targeting ERK phosphorylation by activating the ERK pathway with a constitutively active form of MEK (XREF_FIG)."
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"We next sought to determine how CYLD negatively regulates the ERK signaling pathway in order to mediate NTHi induced IL-8 expression."
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"In addition, we further investigated the detailed mechanism by which CYLD negatively regulates the ERK signaling pathway in a DUB activity dependent or independent manner."
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"Interestingly, CYLD suppresses NTHi induced ERK activation by upregulating another negative regulator, MAP Kinase Phosphatase-1 (MKP-1)."
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"Collectively, it is evident that CYLD specifically inhibits the activation of ERK induced by bacterial pathogen in both human and mouse cells."
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