IndraLab

Statements

TNF increases the amount of GPR68. 15 / 15
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"We further show that the proinflammatory cytokine TNF, a major mediator in IBD associated inflammation, induces OGR1 expression in human and murine myeloid cells."
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"We show that OGR1 expression is induced in monocytes by TNF and OGR1 deficiency protects from spontaneous inflammation in the Il-10 KO model."
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"TNF upregulates OGR1 expression for short periods (6-12 h); however, the effect is not sustained for longer periods, after 24 to 48 hours OGR1 expression returns to basal levels."
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"OGR1 expression induced by TNF, PMA, or LPS was prevented by treatment with PI-3 (Akt1/2), MAP, and PKC inhibitors and with NF-kappaB inhibitors AICAR, BAY-11-7082, CAY10512, and SC-514."
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"The stimulation of OGR1 expression by TNF and hypoxia, and subsequent pH sensing activity, may play a role in IBD pathogenesis."
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"The enhancement of TNF- and hypoxia induced OGR1 expression under low pH points to a positive feed-forward regulation of OGR1 activity in acidic conditions, and supports a role for OGR1 in the pathogenesis of IBD."
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"TNF-α, secreted by PDAC cells, enhances expression of GPR68 on CAFs via a mechanism involving cAMP/PKA/CREB signaling; activated GPR68 causes secretion of IL-6 from CAFs and this in turn increases the proliferation of PDAC cells [236]."
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"XREF_BIBR, XREF_BIBR We show that hypoxia enhances TNF mediated induction of OGR1 expression."
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"In a previous study we reported that TNF treatment induced OGR1 expression in MM6 cells and primary human and murine monocytes, and that this process was reversed by the NF-kappaB inhibitors MG132, AICAR, BAY-11-7082, CAY10512, and SC-514 in MM6 cells."
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"XREF_BIBR In thecurrent study we show that hypoxia enhances TNF mediated induction of OGR1 expression, and that this effect was reversed by NF-kappaB inhibition under hypoxic conditions."
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"We previously reported that OGR1 expression was induced in cells of human macrophage lineage and primary human monocytes by TNF and that NF-kappaB inhibition reversed the induction of OGR1 mRNA expression by TNF."
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"Additionally, TNFα induces the expression of OGR1 in cells of human macrophage lineage and primary human monocytes through an NF-κB-mediated mechanism [22, 23]."
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"Here, we report that hypoxia, known to cross-talk with the NF-kappaB pathway, enhanced the TNF mediated induction of OGR1 expression, which was reversed in the presence of NF-kappaB inhibitors."
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"XREF_BIBR We also observed that OGR1 expression is induced in cells of human macrophage lineage and primary human monocytes by TNF, whereby this effect is reversed by inhibition of the key regulator of chronic mucosal inflammation, nuclear transcription factor-kappaB (NF-kappaB)."
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"Short-term expression of GPR68 is induced by the proinflammatory cytokine TNF, which was also shown to function as a major mediator for IBD-associated inflammation."
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