IndraLab
Statements
Lipopolysaccharide activates ERK. 1000 / 1167
|
8
2
1139
reach
"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."
reach
"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]."
reach
"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]."
reach
"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."
reach
"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."
reach
"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]."
reach
"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."
reach
"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)."
reach
"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."
reach
"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."
reach
"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)."
eidos
"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 ) ."
reach
"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."
reach
"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."
reach
"Chronic inflammation occurs in breast tissue due to fat accumulation caused by obesity [10] In this study, lipopolysaccharide (LPS) was used to trigger inflammation; high concentrations of LPS activated TLR4, ERK and NF-kB pathways, leading to IL-6 production and Mcp1 release [11]."
reach
"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."
reach
"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."
reach
"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."
reach
"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]."
eidos
"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 ) ."
reach
"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."
reach
"This result suggests that ESH inhibits the production of inflammatory genes at the transcriptional levels.ESH Inhibits LPS induced Activation of ERK MAPKs such as ERK1/2 and p38 are involved in the signaling pathways leading to the regulation of inflammatory mediators via the activation of transcription factors especially NF-kB."
reach
"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."
reach
"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."
reach
"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."
reach
"Moreover, these reverse effects of ITE were suppressed with the treatment of AhR antagonist CH223191 (Fig. 7G–H), supporting the AhR dependent role in ITE inhibiting the activation of NFκB. Taken together, these results indicated that AhR activation could down-regulate LPS-induced ERK and NFκB signaling in BV2 microglia and thus limit downstream inflammation.In summary, our results illustrated the unbalanced tryptophan metabolism in glaucoma patients and the role of AhR signaling in retinal neuroprotection."
reach
"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."
reach
"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."
reach
"Simultaneously obtained results showed that plant extracts (5–50 μg/mL) substantially diminished the release of NF-κB, the expression of ICAM-1, and the secretion of IL-8 by LPS-stimulated Hs68 fibroblasts (Table 7) and suppressed (25–50 μg/mL) the LPS-induced Erk kinase activation in dermal cells [89]."
reach
"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."
reach
"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."
| PMC
reach
"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]."
reach
"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."
reach
"Ohyama et al. reported that sudachitin (5,7,4′-trihydroxy-6,8,3-trimethoxyflavone), found specifically in Citrus sudachi, blocked LPS-induced calvarial bone destruction by repressing the ERK and JNK pathways and decreasing intracellular reactive oxygen species (ROS) production in osteoclast precursors [12]."
reach
"On the other hand, phosphorylation levels of JNK (Figure 5B) and ERK (Figure 5C) were increased; p-JNK/JNK (Supplementary Figure 3A) and p-ERK/ERK (Supplementary Figure 3B) ratios were also increased and decreased when treating ALOE, indicating that ALOE suppressed the LPS-stimulated activation of ERK (Figure 5C) and JNK (Figure 5B), instead of p38 (Figure 5D) MAPK pathway."
reach
"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)."
reach
"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."
reach
"Although we have no results showing that NF-kB inhibition prevents IL-8 secretion, data from our laboratory show that LPS activates AKT, ERK1/2 and NF-kB (Boza et al., 2016); and it is well documented in the literature that NF-KB regulates the expression of IL-8; although in this case it was because of IL-1beta (Mizuno et al., 2022)."
reach
"It reduces the expression of genes that code the oxidative stress response in the inflammatory gut (Welch et al., 2014), inhibits the LPS-induced activation of ERK 1/2 and p38 MAPK (Yuan et al., 2016), and alleviates cisplatin-induced nephrotoxicity by inhibiting NADPH oxidase and p38 MAPK (Rashed et al., 2011)."
reach
"It is well known that LPS activates several intracellular signaling pathways including the three mitogen activated protein kinase (MAPK) pathways : extracellular signal regulated kinase (ERK), stress activated protein kinase and c-Jun N-terminal kinase (SAPK and JNK) and p38 MAP kinase."
reach
"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
reach
"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."
reach
"Galangin was demonstrated to have anti-inflammatory effect in a different investigation using LPS-stimulated RAW264.7 macrophages, where the compound significantly decreased the production of NO, inducible NO synthase, IL-6, the NF-κB and suppressed the LPS-induced activation of ERK-1/2 and c-Jun N-terminal kinase [107].4.2.3
Antimicrobial activities."
reach
"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."
reach
"We therefore designed FA-functionalized exosomes co-loaded with resveratrol (an anti-inflammatory polyphenol) and celastrol (an immunosuppressive pentacyclic triterpenoid; FA-Exo/R+C), which exhibited powerful anti-inflammatory and immunosuppressive activities against LPS-stimulated macrophages in vitro by regulating NF-κB and ERK1/2 signaling pathways."
reach
"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."
reach
"These results prove that CP treatments exhibit anti-inflammatory effects on suppressed inflammatory chemokines and cytokines by inhibiting pro-inflammatory mediators, including PI3K-p55, Akt, Erk1/2, p38, and NF-κB, in the LPS-stimulated LA4 cells (Figure 4, Figure 5 and Figure 6)."
reach
"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."
reach
"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."
reach
"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."
reach
"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]."
reach
"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."
reach
"DUSP10 negatively regulates lipopolysaccharide-induced macrophage ERK signaling (Zhang et al., 2004) but has not been implicated in CD40 or B cell regulation.To investigate putative DUSP10 roles in CD40 MAPK regulation, we measured ERK, p38, and JNK activation loop phosphorylation levels in control versus DUSP10 KO cells."
reach
"Taken together, these findings demonstrate that RO impedes osteoclast fusion by suppressing RANKL-mediated activation of the ERK/c-fos/NFATc1 axis.3.5
RO blocks inflammation of chondrocytes and enhances chondrocyte autophagy by inhibiting LPS-induced activation of the ERK pathway."
reach
"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."
reach
"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)."
reach
"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
reach
"Results showed that CASP11 significantly downregulated 120 genes and decreased 14 inflammatory pathways, including IL6 signaling pathway, ferroptosis signaling pathway, HMGB1 signaling pathway, NRF2-mediated oxidative stress response, PI3K/Akt signaling pathway, LPS-stimulated MAPK signaling pathway, senescence pathway, NK cell signaling pathway, ERK/MAPK signaling pathway, mTOR signaling pathway, PI3K signaling in B lymphocytes, CXCR4 signaling pathway, production of nitric oxide and ROS in macrophages, and leukocyte extravasation signaling pathway (Figure 3, A and B)."
reach
"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]."
reach
"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]."
reach
"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."
reach
"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."
reach
"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."