IndraLab
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"In ASM cells, MAPKs mediate changes in the profile of gene expression through phosphorylation of intracellular proteins including transcription factors, and TNF-alpha causes activation of the MAPKs, that is, p38, JNK, and ERK1/2, resulting in the regulated expression of a variety of genes involved in excitation-contraction coupling [XREF_BIBR - XREF_BIBR]."
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"Correspondingly, the results of scratch assay, transwell, migration and invasion all proved that the migration and invasion ability of glioblastoma U251 and U87 cells were significantly enhanced, which indicated that TNF-α promoted the activation of NF-κB and ERK pathway, and in turn promoted the migration and invasion ability of glioblastoma cells."
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"TNF-alpha treatment caused an increase in c-Jun N-terminal kinase (JNK), p38 mitogen activated protein kinase (p38 MAPK), and extracellular signal regulated kinase (ERK) activities, whereas PDGF treatment caused an increase in ERKs and p38 MAPK activities without any effect on JNK activity."
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"In contrast, tumor necrosis factor alpha- or interleukin-1 and Toll-like receptor signaling molecules-such as mitogen activated protein kinase and extracellular signal regulated kinase kinase 1, MyD88, and interleukin-1 receptor associated kinase-did not play a role in RANTES activation by H. pylori."
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"To further address precise mechanism by which UCH-L1 suppresses TNFalpha mediated activation of ERK will provide novel insight into the understanding of TNFalpha mediated inflammatory responses in VSMCs, facilitating development of new therapeutic approaches for the treatment of vascular diseases."
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"Previous studies showed that TNF-alpha stimulates ERK activation through EGFR dependent or -independent pathways, and that EGFR independent ERK activation is mediated through the activation of transforming growth factor-beta-activated kinase 1 and tumor progression locus 2 [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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"ERK1/2, which is involved in the regulation of cell proliferation, differentiation, and motility 42, can also be activated by TNF-alpha, and the ERK1/2 pathway is critical for transducing TNF-alpha signaling to increase matrix metalloproteinase production in trabecular meshwork cells 43."
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"The extracellular signal regulated kinase 1/2 (ERK1/2) pathway is activated by TNFalpha and IFNgamma in some cell types and is upregulated in lung tumors [XREF_BIBR - XREF_BIBR], Herein we examine ERK1/2 dependent signaling events in TNFalpha and IFNgamma mediated inflammatory responses by comparing prostaglandin and NO production with cell proliferation in non transformed and tumor derived mouse lung epithelial cell lines using a small molecule inhibitor of MEK1/2 (U0126), an upstream kinase that phosphorylates and activates ERK1/2."
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"Since AKT, NF-kappaB, or ERK1/2 signaling pathways were activated in HCT116 cells by IL-17 and/or TNF-alpha, we tested if inhibitors of AKT (AZD5363), NF-kappaB (Bay11-7082), or ERK1/2 (U0126) signaling pathways could diminish PD-L1 protein expression induced by IL-17 and/or TNF-alpha."
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"Recently, for the first time, it was reported that sanguinarine inhibits osteoclast differentiation and bone resorption by suppressing the tumor necrosis factor ligand superfamily member 11 induced nuclear factor-kappaB and extracellular signal regulated kinase signaling pathways in vitro."
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"Compared with the effect of Dex alone, the phosphorylation levels of p38 MAPK, ERK1/2 and JNK induced by TNF-α decreased by 33, 75, and 63%, respectively, after R406 pretreatment.Next, we used inhibitors of MAPKs in BEAS-2B cells to study the effects of MAPK phosphorylation on GR-Ser226."
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"We studied both apathogenic (Tula and Topografov) and pathogenic (Puumala and Seoul) hantaviruses for their ability to regulate cellular signaling pathways and observed a direct virus mediated down-regulation of external signal regulated kinases 1 and 2 (ERK1/2) survival pathway activity, which was dramatically enhanced by TNF-alpha."
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"Although some information is known about selected changes in chondrocyte gene expression in response to TNFalpha activated MEK and ERK signalling, the overall impact of this pathway on changes to the chondrocyte gene expression and the downstream transcriptional mechanisms mediating these changes has been poorly defined."
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"The suppression of TNF-α by HP-PRRSV was mediated through inhibiting the ERK signaling pathway, and nsp1β and nsp11 were responsible for the inhibitory effect on TNF-α production induced by HP-PRRSV and the differential TNF-α production in PAMs (He et al., 2015; Hou et al., 2012a)."
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"As shown in the representative blot in XREF_FIG and the densitometric analysis of 3 separate blots from 3 different experiments shown in XREF_FIG, TNFalpha induced the activation of ERK 1/2 with a time course of increasing activation out to at least 5 h. Immunoblotting to quantify total ERK 1/2 showed that there was no change in the amount of total ERK 1/2 protein during the incubation period."
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"Furthermore, when cells were incubated for 5 minutes with dexamethasone and TNF-α, Western blots showed an inhibiting effect of dexamethasone on TNF-α-induced ERK activation (188±16% of control after TNF-α alone versus 125±5% of control after dexamethasone and TNF-α treatment, n = 4, * P <0.05 compared to TNF-α alone, xref )."
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"The aims of this study were to investigate whether fibronectin (FN) or the inflammatory cytokines interleukin-1alpha (IL-1alpha) and tumor necrosis factor-alpha (TNF-alpha) activate JNK, ERK, and AP-1 activity in HSC and induce the gene expression of the matrix metalloproteinase transin."
eidos
"By binding to the TNF receptor on the osteocyte surface , TNF-alpha activates the ERK1 / 2 , P38 and Jun kinase ( JNK ) MAPK signaling pathways and / or the transcription factor nuclear factor-kappa B ( NF-kappaB ) , which enhances RANKL expression in osteocytes and consequently promotes alveolar bone resorption [ 34 , 35 ] ( Fig. 2 ) ."
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"IL-1β and TNF-α mainly activate the nuclear factor-κB pathway [32, 33], while IL-6 and IL-10 exert their complex actions through multiple pathways like the Janus kinase 2/signal transducers and activators of transcription 3 pathway and the p38 mitogen-activated protein kinase/extracellular signal-regulated kinase pathway [34, 35]."
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"In spinal cord outer lamina II neurons, TNF-alpha increases spontaneous EPSC frequency but not amplitude via pre-synaptic transient receptor potential subtype V1 (TRPV1)-mediated glutamate release that is dependent on adenylyl cyclase (AC), PKA, and the extracellular signal regulated kinase (ERK) in pre-synaptic terminals."
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"Additionally, by activating TNFR1 in airway smooth muscle, TNF-alpha triggers extracellular signal regulated kinase (ERK) and p38 mitogen activated protein kinases (MAPKs) signaling pathway and transcription factors to turn on a variety of genes (interleukins) that mediate inflammatory and immune responses [XREF_BIBR]."
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"By binding to the TNF receptor on the osteocyte surface, TNF-α activates the ERK1/2, P38 and Jun kinase (JNK) MAPK signaling pathways and/or the transcription factor nuclear factor-kappa B (NF-κB), which enhances RANKL expression in osteocytes and consequently promotes alveolar bone resorption [ xref , xref ] (Fig. xref )."
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"Specifically, TNFRI206-211 had no effect on the TNF-induced activation of ERK, JNK, and NF-κB. Likewise, a TNFR domain responsible for connecting TNF-JNK signaling may be identified and characterized, which would help in the design of specific inhibitors of JNK but not p38 or ERK to influence TNF-mediated effects."
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"Notably, TNF-α induces ADAM17 and Src dependent EGFR activation and initiates the extracellular signal-regulated kinase (ERK)-dependent guanine nucleotide exchange factors (GEF)-H1 and RhoA signaling pathway, suggesting a mechanistic link between inflammatory and proliferative pathophysiology [27]."
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"In contrast, our study shows that OTUB1-deficiency in hepatocytes and the subsequent accelerated degradation of c-IAP1 (i) augmented Lm- and TNF-induced ERK activation without affecting canonical and noncanonical NF-κB activation and expression of NF-κB-dependent antiapoptotic genes (ii) induced RIPK1 and MLKL-dependent necroptosis."
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"Although TNF-alpha was a considerably stronger activator of NF-kappaB than PMA in MEFs and HEK293 cells, TNF-alpha poorly induced c-Fos, which can be explained by the inability of TNF-alpha to induce strong and sustained activation of ERK and the essential downstream transcription factors Elk-1 and CREB."
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"This study investigated in 3T3-L1 adipocytes, the capacity of (-)-epicatechin to inhibit TNFalpha triggered deregulation of signaling pathways (MAPKs ERK1/2, JNK and p38, and transcription factors NF-kappaB, AP-1, and PPARgamma) that regulate genes involved in inflammation and insulin resistance."
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"XREF_BIBR, XREF_BIBR HIF-1alpha is highly expressed in synovial fibroblasts and infiltrating macrophages in the inflamed RA joint, where it enhances TNF-alpha- and IL-1beta-driven activation of the p38 and extracellular signal regulated kinase signaling pathways, resulting in increased IL-33 expression."
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"TNF-alpha can simultaneously activate several MAPKs family members (P38 MAPK, ERK, and JNK) and was used to treat HeLa cells at the concentration of 10 ng/ml for 2 h. TTP became extensively diffused in the cytoplasm and did not localize to PBs (XREF_FIG), while the focal pattern of PBs was preserved under TNF-alpha stimulation (XREF_FIG)."
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"Although ERK and AKT inactivation was also noted in the presence of SHH inhibitors, these kinases were not significantly activated upon TNF-alpha stimulation of IEC-6 cells (in colon cancer cells HCT-116, ERK and AKT were significantly activated by TNF-alpha and significantly inactivated by SHH inhibitors; data not shown)."
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"XREF_BIBR XREF_BIBR - XREF_BIBR Studies have found that the ERK pathway is not only involved in the regulation of cell responses induced by growth factors, but is also activated by TNF-alpha, IL-1, and others, and plays an important regulatory role in cellular responses induced by stimulation of stress and bacterial products."
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"Microarray technology has been used to study the effects of TNF-alpha stimulated MEK and ERK signaling on global chondrocyte gene expression, resulting in the discovery that among the TNF-alpha modulated genes, proinflammatory genes are MEK and ERK independent, while genes encoding proteins with proteinase activity and HA binding activity, contributing to matrix catabolism, are MEK and ERK dependent."
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"Analyses of Nfkb1 SSAA and SSAA macrophages, in which the IKK target serine residues on NF-kappaB1 p105 are mutated to alanine, revealed that TPL-2 regulates TNF production independently of IKK induced NF-kappaB1 p105 proteolysis and ERK1/2 activation, while still associated with NF-kappaB1 p105 and ABIN-2 [XREF_BIBR]."
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"We have previously shown that tumor necrosis factor (TNF) induced the up-regulation of the sialyltransferase gene ST3GAL4 (alpha2,3-sialyltransferase gene) BX transcript through mitogen- and stress activated kinase 1/2 (MSK1/2), extracellular signal regulated kinase (ERK) and p38 mitogen activated protein kinase (MAPK) signaling pathways."
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"Many independent researchers using cell based studies and different animals models established that TNF-alpha induces the activity of MAPKs (ERK1/2, p38 and JNK) and other kinases such as IKKbeta, PKC, mTOR and its downstream effector, S6K which in turn phoshorylate IRS1 at Ser 307 resulting in interruption of insulin signaling XREF_BIBR XREF_BIBR XREF_BIBR XREF_BIBR XREF_BIBR XREF_BIBR XREF_BIBR XREF_BIBR."
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"Owing to TNF-alpha ' effects on ATM, ERK, p38 and p65 activation (XREF_SUPPLEMENTARY), the inhibition of ERK or p38 decreasing TNF-alpha induced p65 activation (XREF_SUPPLEMENTARY) indicate that ATM might play a potential role in TNF-alpha induced ERK and p38-NF-kappaB activation."
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"RESULTS: We studied both apathogenic (Tula and Topografov) and pathogenic (Puumala and Seoul) hantaviruses for their ability to regulate cellular signaling pathways and observed a direct virus-mediated down-regulation of external signal-regulated kinases 1 and 2 (ERK1/2) survival pathway activity, which was dramatically enhanced by TNF-α."
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"TNF-induced anti-apoptotic pathways include PI3K/AKT, ERK/MAPK, and nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB), whereas pro-apoptotic TNF induced-pathways include p38 MAPK and stress-activated protein kinase/c-Jun NH2-terminal kinase (SAPK/JNK) [15,16,17]."
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"Through binding to and activating TNFR1 on VEC surface, TNFalpha can promote the activation of transcription factor nuclear factor- kappaB (NF-kappaB) and p-38 and ERK1/2 MAPKs (Mitogen activated protein kinases) signaling pathways, thereby up-regulating the expression of cell adhesion molecules (CAMs), including intracellular adhesion molecule-1 (ICAM-1) and E-selectin, which are involved in the processes of leukocyte attachment and transmigration."
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"Hantaviruses and TNF-alpha act synergistically to induce ERK1/2 inactivation in Vero E6 cells.Hantaviruses (Family Bunyaviridae, Genus Hantavirus) are viruses which chronically infect rodents and insectivores with no apparent disease but in humans they cause two major clinical symptoms: HFRS in Eurasia and hantavirus cardiopulmonary syndrome (HCPS) in the Americas."
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"One kinase of the MAPK, p38, was reported to be increased in animal models of neuropathic pain.15 TNF-α activates multiple signaling pathways, including the p38 MAPK pathway,16 which is recognized as an important regulator of inflammatory pain,17 although TNF-α can also activate ERK or c-JUN of MAPK."
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"Furthermore, TNFalpha activation of Erk was abolished by a dominant negative Rac mutant, Rac17N, or by an activated Rac mutant, Rac12V. These findings suggest that Rac is activated by a mechanism that is at least partly dependent on PI3K in TNFalpha stimulated cells and plays a critical role in activation of the Erk signaling pathway."
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"Interestingly, while the activation of p38 MAPK by IL-1β, fibroblast growth factor 1 (FGF-1), or FGF-2 was sensitive to dexamethasone or fluticasone propionate (Fernandes, et al., 1999; Tran, et al., 2005; Willems-Widyastuti, et al., 2013), the activation of ERK1/2 MAPK by TNF was found to be insensitive to GCs (Fernandes, et al., 1999; Robins, et al., 2011)."