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Lipopolysaccharide activates ERK. 699 / 717
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"Furthermore , we observed that LPS stimulation can markedly increase p38 , ERK1 / 2 , and JNK phosphorylation ; however , Farrerol markedly decreased the ERK1 / 2 and JNK1 / 2 phosphorylation but had no effect on the p38 phosphorylation in LPS-stimulated RAW264.7 cells ( Figure 7A-D ) ."
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"Accordingly, depletion of Arl11 impaired both LPS stimulated pro inflammatory cytokine production by macrophages, and their ability to control intracellular replication of Salmonella LPS stimulated activation of extracellular signal regulated kinase (ERK) and p38 mitogen activated protein kinase (MAPK) was substantially compromised in Arl11 silenced macrophages."
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"LA also alleviates LPS induced acute lung and kidney injury through NF-kappaB and p38 and ERK mitogen activated protein kinase (MAPK) signaling and attenuates pertussis toxin induced autoimmune encephalomyelitis by reducing the production of tumor necrosis factor-alpha and interferon-gamma in vivo [XREF_BIBR, XREF_BIBR, XREF_BIBR]."
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"An intriguing finding is that zerumbone did not have an effect on lipopolysaccharide (LPS)-triggered activation of mitogen activated protein kinases (MAPKs; extracellular signal regulated kinase 1/2, c-Jun N-terminal kinase1/2, p38MAPK) or key transcription factors (activator protein-1 and nuclear factor kappaB; NF-kappaB), while it targeted a post-transcriptional mechanism."
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"Because IL-6 activates ERK1/2, which has been reported to be a kinase for STAT3 phosphorylation on Ser 727, and we have previously reported that GW501516 prevents LPS induced ERK1/2 activation in adipocytes, we evaluated the effect of the PPAR-delta agonist on the activation of this kinase."
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"Recently we demonstrated that lipopolysaccharide (LPS) promotes activation of the Ras and ERK cascade in medfly hemocytes and that phagocytosis of Escherichia coli by insect hemocytes is mediated by an integrin dependent process via the activation of FAK and Src complex (J Biol Chem 273 (1998) 14813; FEBS Letters 496 (2001) 55)."
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"The present study demonstrated that lutein and zeaxanthin inhibited the secretion of IL-8 induced by LPS through the activation of JNK1/2 and NF-kappaB signal pathway, but not p38 and ERK pathway; this is consistent with the animal study, which showed that lutein inhibited the activation of NF-kappaB in the iris-ciliary body in LPS induced uveitis and in cultured macrophages [XREF_BIBR, XREF_BIBR]."
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"In this study, we examined the inhibitory effect of diosmetin on MAP kinase pathway and NO production activated by LPS in raw 264.7 cells, and as a result, diosmetin inhibits the LPS induced activation of ERK, p38 and JNK pathway and it also inhibits iNOS expression and NO production."
| PMC
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"Because ligation of TLR4 triggers the activation of MAP kinase and NF-kappaB, leading to production of proinflammatory cytokines through the MyD88 dependent pathway, we investigated the activation of MAP kinase such as JNK, p38, and ERK1/2 in macrophages treated with LPS or 2,000 kDa gamma-PGA."
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"Additional evidence suggesting that P2 receptors are involved in LPS mediated macrophage activation comes from the work of Hu et al. [XREF_BIBR] wherein it was shown that pretreatment of RAW 264.7 macrophages with P2 receptor antagonists, oATP or pyridoxal-phosphate-6-azophenyl-2-4-disulfonic acid (PPADS), inhibited LPS stimulated NO production and/or iNOS expression and attenuated LPS activation of NF-kappaB and ERK-1/2."
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"Further study of the signaling mechanisms revealed that although LPS can activate both Erk MAP kinase and PI3 kinase pathways, only blocking of PI3K abolished both Bcl-x upregulation and the enhanced survival phenotype, suggesting that the PI3K signaling mediated the upregulation of Bcl-x for the LPS induced pro survival in GM-DCs."
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"Moreover, ambroxol significantly alleviated LPS induced the influx of inflammatory cells and the extracellular signal regulated kinase 1/2 (Erk 1/2) expression in lung tissues, and inhibited increases in the mRNA expression of the pro inflammatory cytokines tumor necrosis factor (TNF)-alpha, CCL-2 (monocyte chemotactic protein-1), KC (keratinocyte cell protein) and interleukin (IL)-1beta in lung tissues."
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"LPS have been reported to activate ERKs in some cell types, but no such effects were observed in our experiments with the rat liver epithelial WB-F344 cells, even when we used LPS isolated from Salmonella typhimurium, a serotype producing LPS known to induce significant biological responses."
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"Notably, Ntcp and Bsep RNA levels were maintained at 78Ϯ50% and 60Ϯ46% of control levels, respectively.following authors have indicated they have no relationships to disclose: Claus Hellerbrand, Marcus Mü hlbauer, Martin Fleck, Thomas Weiss, Matthias Froh, Sabine Hoves, Jü rgen Schö lmerich956 ENHANCED LPS-STIMULATED ERK1/2 ACTIVATION AND TNFÁ SECRETION BY RAT KUPFFER CELLS AFTER CHRONIC ETHANOL FEEDING IS MEDIATED VIA INCREASED PRODUCTION OF REACTIVE OXYGEN SPECIES (ROS) BY NADPH OXIDASE Varsha Thakur, Megan R. McMullen, Qifang Wang, Laura E. Nagy, Case Western Reserve University, Cleveland, OHBackground: Production of ROS by Kupffer cells (KC) contributes to the development of chronic ethanol (EtOH)-induced liver injury."
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"In addition, Cortex Phellodendri inhibited inducible nitric oxide synthase (iNOS), activated nuclear factor-kappaB (NF-kappaB) by degradation and phosphorylation of IkappaBalpha, and attenuated phosphorylation of mitogen activated protein kinases such as ERK1/2, p38, and JNK in mice treated with lipopolysaccharide [XREF_BIBR]."
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"The phosphorylation of intracellular signaling molecules of NF-kB pathway, including phosphoinositide 3-kinase (PI3K)/p85, AKT, inhibitor of NF-kappaB (IkappaBalpha) kinase alpha/beta (IKKalpha and beta) and IkappaBalpha, and TRAF family member associated NF-kappaB activator (TNAK)-binding kinase 1 (TBK1), a key intracellular signaling molecule of IRF-3 pathway, as well as MARK pathways were activated by extracellular LPS, as expected, in WT Raw264.7 macrophages, while their activations, with the exception of ERK, were reduced in p204 deficient Raw264.7 macrophages treated with LPS."
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"To study the effect of EGFR activation on the generation of TNF-alpha and the occurrence of cardiac dysfuncetion during sepsis, PD168393 and erlotinib (both are EGFR inhibitors) were applied to decreased the production of TNF-alpha and phosphrylation of ERK1/2 and p38 induced by LPS in cardiomyocytes."
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"ERK1/2 (Immunoblot) in RAW cells treated with LPS (1ug/ml) in the presence and absence of LDN.The docked conformation of naltrexone at the binding interface of RBD and ACE2 complex obtained from AutoDock (A) and interface amino acid residues involved in non bonded contacts are labelled (B)."
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"Further analysis showed that LPS induced a more dramatic activation of ERK and cell proliferation in Cx43 +/+ spleen cells, which was associated with a higher pro oxidative state, as indicated by the increased NADPH oxidase 2 (NOX2), TXNIP, p38 activation and protein carbonylation."
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"The phosphorylation of cPLA 2 alpha at 1 hour and phosphorylation of ERK1/2 at 10 minutes were significantly prevented in mice treated with SC-215 prior to LPS challenge, but the induction of phospho-p38 at 10 minutes were not affected upon SC-215 pretreated and remained similar to LPS challenge values (XREF_FIG)."
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"Accumulating evidence suggests that LPS can activate nuclear factor-kappa B (NF-kappaB) and three mitogen activated protein kinase (MAPK) pathways, inculding the c-Jun NH2-terminal kinase (JNK), extracellular signal regulated kinase (ERK), and p38 pathways, which result in the overexpression of inflammatory mediators such as tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), NO and prostaglandin (PG) E 2."
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"Given the importance of the canonical form of transcription factor NF-kappaB in both the production of the components of the oxidative stress response (p47 and p67 are regulated by NF-kappaB), and in the regulatory effects of ROS in activating microglia (NF-kappaB controls ERK activity induced by LPS signaling, XREF_FIG), inhibitors of the canonical pathway of NF-kappaB should provide strong evidence of the role of oxidative stress responses in PD."
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"We have previously shown that inducible inflammatory mediator production is inhibited by a post-transcriptional mechanism, since mycolactone does not modulate the LPS dependent activation of ERK, JNK, p38 MAPK or NFkappaB and induced levels of mRNA are maintained or even enhanced XREF_BIBR."
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"In a subsequent study, we demonstrated that p38 kinase, rather than ERK1/2, was activated in Dami cells by LPS in dose- and time dependent manner, suggesting that the phosphorylation of ERK and p38 is regulated by different mechanisms and that p38 kinase plays the key role in the response of Dami cells to LPS stimulation (XREF_FIG)."
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"In BV2 cells ( a murine microglial cell line ) , LPS increases the Ca2 + concentration and upregulates CaMKII phosphorylation , thus inducing ERK1 / 2 and NF-kappaB phosphorylation , which stimulate microglial activation and the expression of pro-inflammatory cytokines and enzymes ( Wu et al ., 2018 ) ."
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"Recently we demonstrated that lipopolysaccharide (LPS) promotes activation of the Ras and ERK cascade in medfly hemocytes and that phagocytosis of Escherichia coli by insect hemocytes is mediated by an integrin dependent process via the activation of FAK and Src complex (J Biol Chem 273 (1998) 14813; FEBS Letters 496 (2001) 55)."
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"To examine the negative functional role of TAM receptors on microglia in response to TLR activation, we activated TLR4 on primary cultured microglia with LPS and found that LPS stimulation caused rapid activation of both ERK1/2 and p38 in TKO cells compared to WT microglia (XREF_FIG)."
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"It has been repeatedly observed that ' activation ' of macrophages and other cells can lead to an accumulation of Anx-A1 at the plasma membrane where it can (for example) block EGF XREF_BIBR and LPS induced ERK activation XREF_BIBR and undoubtedly fulfil other intracellular roles."
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"To determine the effect of amentoflavone on LPS activated ERK activity, immunoprecipitated ERK (prepared from RAW264.7 cells (5 x 10 6 cells/mL) that had been treated with LPS in the presence or absence of amentoflavone) was incubated with MBP according to the manufacturer 's instructions."
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"The effects of basolateral LPS to activate ERK and inhibit HCO (3) (-) absorption were eliminated in MTALs from TLR4 (-/-) and myeloid differentiation factor 88 (MyD88) (-/-) mice but were preserved in MTALs from TIR (Toll and interleukin -1 receptor) domain containing adapter inducing interferon-beta (Trif) (-/-) mice."
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"In mKC, LPS treatment resulted in transient and rapid increase of kinase activity of ERK1/2 that phosphorylated their specific substrate ELK-1, with maximal value at 30 minutes and a return near to baseline within 2 hours, and LPS induced ERK1/2 activity from LPS concentration of 10 pg/ml to the top activity at 100 ng/ml."
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"LPS activates ERK1 / 2 , JNK , and p38 MAPK , which ultimately control the activity of transcription factors regulating the expression of inflammation modulators , such as induced NO synthase ( iNOS ) , cyclooxygenase-2 ( COX-2 ) , TNF-alpha , IL-1alpha , IL-1beta , and IL-6 [ 44 ] ."
| PMC
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"The LPS tolerance in DOK3 deficient cells was accompanied by significant upregulation of SHIP1, IRAK-M, and SOCS1 suggesting that the enhanced ERK and NF-kappaB activation, induced by the initial LPS stimulation, primes the cells for rapid induction of tolerance upon re-challenge."
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"These results suggested that CuEO exerted anti-inflammatory effects in LPS stimulated RAW 264.7 cells via inhibition of NF-kappaB and mitogen activated protein kinases ERK and JNK signaling; the chemical could be used as a source of anti-inflammatory agents as well as dietary complement for health promotion."
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"LPS activated Akt1-/- macrophages exhibited increased ERK1/2 activation (XREF_SUPPLEMENTARY) but no change in IkBalpha degradation (XREF_SUPPLEMENTARY), suggesting that Akt1 plays an inhibitory role in early TLR4 signals but its ablation is not sufficient to suppress pro inflammatory cytokine production at the early stages of endotoxemia."
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"Signaling cascade analysis showed that LPS induced activation of Erk, JNK, p38 mitogen-activated protein kinase (MAPK), and NF-κB, and RA treatments attenuated the activation of the three MAPKs and NF-κB. Moreover, cotreatment with RA and Erk, JNK, p38 MAPK, or NF-κB inhibitors further downregulated the mRNA expression of TNFα, IL-8, and iNOS, and decreased the production of TNFα, IL-8, and NO by A7r5 cells."
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"To confirm that LPS-induced ERK activation was linked to NF-kB signaling, we monitored activation of NF-kB and ERK over time in RAW264.7 cells preincubated with or without 1 µM SC-1, an inhibitor of ERK activation, for 3 h and then treated with 1 μM LPS for 15–45 min using western blotting."
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"As shown in Figures XREF_FIG, XREF_FIG, and XREF_FIG, LPS treatment caused a marked increase in the phosphorylation of ERK1/2, JNK1/2, and p38 MAPK proteins at 5, 15, and 5min, respectively, whereas LPS induced ERK1/2, JNK1/2, and p38 MAPK phosphorylation was significantly inhibited by TS and GA treatment."
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"ERK1/2 (Immunoblot) in RAW cells treated with LPS (1ug/ml) in the presence and absence of LDN.Figure 2. : The docked conformation of naltrexone at the binding interface of RBD and ACE2 complex obtained from AutoDock (A) and interface amino acid residues involved in non bonded contacts are labelled (B)."
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"SME inhibited LPS-induced phosphorylation of ERK after 15–30 min, and the amount of p-ERK had returned to the basal level after 60 min in LPS-stimulated RAW264.7 cells pretreated with SME
SME suppresses expression of signaling components involved in LPS-induced activation of ERK in RAW264.7 cells."
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"These results can be compared with those published in 2015 by Kim et al. [88] who showed that BoNT/A inhibited LPS-upregulated NO production in RAW264.7 macrophages by blocking the activation of ERK and p38.Recently, many papers have shown that the inhibition of the MAPK family members (namely p38 and ERK1/2) leads to lower rates of neuropathy in animal models, down-regulated pro-nociceptive factors and enhanced opioid efficiency [84,89,90,91,92,93,94,95,96]."
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"Using a number of approaches : mouse embryonic fibroblasts (MEF) from wild-type (WT), beta-arrestins knockouts (KO), beta-arrestins 1 and 2 double KO, and MEFs with reconstituted WT beta-arrestins in the double KO cells, RNA interference (siRNA) specific knockdown of beta-arrestins, and overexpression of WT beta-arrestins, it was demonstrated that beta-arrestin 2 positively regulates LPS induced ERK 1/2 activation and both beta-arrestins 1 and 2 negatively regulate LPS induced NFkappaB activation."
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"The present study indicated that p38 and ERK1/2 were activated and translocated into nucleus in astrocytes by LPS exposure with different patterns, i.e., p38 was firstly activated at 30min and reached peak at 2h while ERK1/2 activated at 1h and reached peak at 3h, while inhibition of p38 and ERK1/2 attenuated the changes of GS expression induced by LPS."
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"Second, the blockade of Src like tyrosine kinases or Raf-1 inhibits LPS induced ERK activation; this inhibition suggests that the Raf-1/MEK/ERK signaling pathway is present and activated by Src like tyrosine kinases and Raf-1-dependent mechanisms, which do not require Ksr1 as a scaffold."
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"ERK activation has been previously shown to be critical for ICAM-1 expression, and in accordance with that report, we found that LPS induced ERK activation is critical for ICAM-1 expression in MDA-MB-231 cells and for their adhesion to monocytes (XREF_FIG), Several reports have suggested that NF-kappaB lies downstream of ERK, thus regulating ICAM-1 expression."
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"For example, CpG DNA upregulates the expression of the cellular inhibitor of apoptosis (c-IAP) 1 and 2, while it downregulates the levels of active caspase-3 in a PI3K dependent manner; HIV infected DCs become resistant to NK induced TRAIL mediated apoptosis due to the upregulation of the cellular-Flice-like inhibitory protein and c-IAP2; LPS activates ERK, which regulates DC survival."
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"We show that treatment of differentiated THP-1 cells with purified Stx1 resulted in prolonged activation of c-Jun N-terminal kinase (JNK) and p38 mitogen activated protein kinase (MAPK) cascades, and lipopolysaccharides (LPS) rapidly triggered transient activation of JNK and p38 and prolonged activation of extracellular signal regulated kinase cascades."
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"Anti-inflammatory effects of scoparone in a rat model of colitis have also been reported (151), while in BV2 microglial cells, scoparone attenuated LPS-induced neuroinflammatory responses by blocking interferon regulatory factor 3 (IRF3) and extracellular signal-regulated kinase (ERK) activation (126)."
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"In the lipopolysaccharide induced inflammatory response of rat embryonic ventricular myocardial cells (H 9 C 2 cells), our group also found [XREF_BIBR] that SPRC prevented nuclear factor-kappaB (NF-kappaB) activation and suppressed LPS induced extracellular signal regulated kinase 1/2 (ERK1/2) phosphorylation and intracellular reactive oxygen species (ROS) production."
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"To determine the inhibitory effects of AG or U0126 on LPS activated ERK or IKKepsilon enzyme activities, immunoprecipitated phospho-ERK or IKKepsilon prepared from RAW264.7 cells (5 x 10 6 cells/mL) treated with LPS (1mug/mL) for 30 (ERK) or 10 (IKKepsilon) min were incubated with AG or U0126 in the presence or absence of substrate protein [myelin basic protein (MBP)] or immunoprecipitated IRF-3 from unstimulated RAW264.7 cells, according to the manufacturer 's instructions."
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"Cholesterol extraction from the intact macrophage with methyl-beta-cyclodextrin was sufficient to activate ERK, recapitulating the LPS-IkappaB kinase-p105-MEK-ERK cascade, whereas both it and the alternate raft disrupting agent nystatin blocked subsequent LPS activation of the ERK cascade."
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"Pretreating murine macrophages (RAW 264.7) with luteolin inhibited LPS stimulated TNFalpha and IL-6 release, which was associated with blockage of LPS induced activation of nuclear factor kappa B (NF-kappaB) and mitogen activated protein kinase (MAPK) family members ERK, p38, and JNK [XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR]."
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"Eicosanoid signaling is upregulated by lipopolysaccharide (LPS), pro inflammatory cytokines interleukin (IL)-1beta, IL-6 and tumor necrosis factor (TNF)-alpha, nuclear factor kappa-B (NF-kappaB), and mitogen activated protein kinases (MAPK) p38, extracellular signal regulated kinase (ERK) and c-Jun N-terminal kinases (JNK), all of which are all important mediators of neuroinflammation [XREF_BIBR, XREF_BIBR, XREF_BIBR]."
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"Another sigma-1 receptor agonist, (+)-pentazocine, reduced the release of tumor necrosis factor α (TNF-α), interleukin 10 (IL-10), monocyte chemoattractant protein-1 (MCP-1), and nitric oxide (NO) and inhibited LPS-induced activation of ERK and c-Jun N-terminal kinase (JNK) pathways (Zhao et al., 2014)."
| PMC
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"Many MPs are capable of inducing inflammatory pathways in DCs mediated by signaling via the extracellular signal regulated kinase 1/2 (ERK1/2) which can be activated by growth factors, cytokines, stress factors, viral infections, carcinogens, and bacterial components such as, lipopolysaccharide."
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"We found that SPRC prevented nuclear factor-kappaB (NF-kappaB) activation assessed by NF-kappaB p65 phosphorylation and IkappaBalpha degradation, suppressed LPS induced extracellular signal regulated kinase 1/2 (ERK1/2) phosphorylation and intracellular reactive oxygen species (ROS) production."
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"A competitive antagonist of vasoconstrictor effects of 20-HETE, 20-hydroxyeicosa-6 (Z),15 (Z)-dienoic acid, 20-HEDE (30 mg/kg, s.c.; 1 h after LPS) prevented the effects of 5,14-HEDGE on blood pressure, heart rate, expression and/or activity of sEH, CYP2C23, and ERK1/2 as well as TNF-alpha and IL-8 levels in rats treated with LPS."
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"Eicosanoid signaling is upregulated by lipopolysaccharide (LPS), pro inflammatory cytokines interleukin (IL)-1beta, IL-6 and tumor necrosis factor (TNF)-alpha, nuclear factor kappa-B (NF-kappaB), and mitogen activated protein kinases (MAPK) p38, extracellular signal regulated kinase (ERK) and c-Jun N-terminal kinases (JNK), all of which are all important mediators of neuroinflammation [XREF_BIBR, XREF_BIBR, XREF_BIBR]."
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"Collectively, these data support the novel concept that TLR4 activation in ASM elicits changes in ASM function that are regulated by opposing effects of MAPK signaling, wherein LPS induced ERK1/2 activation mediates NF-kappaB-dependent proasthmatic like changes in ASM function, whereas coactivation of p38 MAPK serves to homeostatically downregulate the proasthmatic effects of ERK1/2 activation."
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"Moreover, IL-21 inhibited LPS-mediated secretion of inflammatory cytokines, probably by downregulating the ERK1/2, in RA-SF MΦs. Conclusion :For the first time, we indicated that IL-21 inhibits LPS-mediated cytokine production in RA-SF MΦs, and impairs pro-inflammatory activity of M1-like macrophages, hereby exerting anti-inflammatory effects on RA."
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"At concentrations of 0.5, 0.75, and 1mg/mL, treatment with BPTS inhibited levels of expression of LPS induced NF-kappaB and MAPKs (ERK, JNK, and p38) as well as production of proinflammatory mediators, such as nitric oxide (NO), prostaglandin E 2 (PGE 2), tumor necrosis factor-alpha (TNF-alpha), and interleukin-6 (IL-6) by LPS."
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"The LPS stimulation of macrophages activates several intracellular signaling pathways that include the IκB kinase (IKK)–nuclear factor kappa B (NF-κB) pathway and three classical mitogen-activated protein kinase (MAPK) pathways: extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 [18,19,20]."
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"d-GalN/LPS treatment resulted in a marked inflammatory cytokine release and stimulated the activation of signal transducer and activator of transcription (STAT) 3, c-Jun N-terminal kinases (JNK) and extracellular signal-regulated kinase (ERK) signaling comparably in the hepatic compartment of Bcl-3 Hep and WT mice."
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"ERK, JNK, and p38 MAP kinases are activated by LPS in microglia and inhibition of a respective kinase with pharmacological inhibitors : CEP11004 or CEP-1347 reduced cytokine production in LPS stimulated human and murine microglia cultures [XREF_BIBR, XREF_BIBR] or exposed to neurotoxic peptide Abeta1-40 [XREF_BIBR]."