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Lipopolysaccharide inhibits NFKBIA. 356 / 357
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"In the present study, an analysis of the whole cell extracts showed that the P.g. LPS induced IkappaBalpha degradation in fibroblasts was paralleled by a P.g. LPS induced increase in CatB in the late culture period; furthermore, the P.g. LPS induced IkappaBalpha degradation was prevented by CA-074Me pretreatment (XREF_FIG)."
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"Furthermore, treatment with the PKC inhibitor abrogated LPS induced IkappaBalpha degradation and NF-kappaB activation, while treatment with the PTP inhibitor enhanced LPS induced IkappaBalpha degradation and NF-kappaB activation in p-AMs, suggesting that PKC and PTP are regulators of LPS induced IkappaBalpha degradation and NF-kappaB activation."
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"More importantly, pretreatment with the PTP inhibitor, but not the PKC inhibitor, blocked the effect of aspirin on LPS induced IkappaBalpha degradation and NF-kappaB activation, suggesting modulating the activity of PTP and PKC and subsequently inhibiting the activation of NF-kappaB may contribute to the anti-inflammatory effect of aspirin on ALI."
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"SUPPRESSION OF INFLAMMATORY THROUGH MULTIPLE STEPS BY GARCINOL147p38 MAPK Was Involved in the Inhibition of LPS Induced IkBa Degradation Brought About by GarcinolBased on the result that p38 MAP kinase activity was inhibited by garcinol, we subsequently determined whether p38 MAPK played a role in stabilizing IkBa in LPS activated macrophages."
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"Previous studies have shown [XREF_BIBR, XREF_BIBR], cilostazol inhibits proinflammatory factor (including remnant lipoprotein particle, TNFalpha and LPS)-stimulated increases in IkappaBalpha degradation and NF-kappaB p65 activity, and thus, suppresses the productions of inflammatory cytokines."
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"To rule out the possibility that this decrease was due to the loss of PP4 's known negative regulation of LPS induced NFkappaB activation XREF_BIBR, we examined LPS induced IkappaBalpha degradation in WT and CD23 cre PP4 F/F B cells but found no abnormalities in the mutant cells (XREF_SUPPLEMENTARY)."
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"OXO pretreatment significantly suppressed the amount of c-Jun and c-Fos in a dose dependent manner.OXO fails to suppress LPS induced IkBa degradation and p65 nuclear translocationAlthough NF-kB is a multifunctional transcription factor, it is an important target for controlling inflammation as the transcription of many pro inflammatory molecules depends on the activation of NF-kB12."
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"However, as the precise timing and mechanism of LPS and nigericin activation of the Nalp3 (NLRP3) inflammasome is poorly understood, it is also possible that the lack of activated caspase-1 was due to altered TLR signaling in heat shock conditions, as reflected by heat shock 's inhibitory effect on LPS mediated IkappaB-alpha breakdown (data not shown)."
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"We found that SC extract attenuated LPS induced IkappaB-alpha degradation as well as nuclear translocation of p65 in BV-2 microglia, indicating that SC extract inhibits iNOS and TNF-alpha gene expression in microglia and may be involved in the inhibition of NF-kappaB activation as a possible mechanism."
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"Treatment with LPS induced IkappaBalpha degradation in control CMT-93 cells expressing an empty vector, whereas CMT-93 cellsexpressing the Smad6 beta-sheet subregion did not show IkappaBalpha degradation upon LPS treatment, similar to the results of TGF-beta1 pre-treatment for 2h (Fig XREF_FIG)."
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"In the present study, we observed that LPS challenge induced the degradation of IkappaB-alpha and activation of NF-kappaB in vitro, and the activation of NF-kappaB signaling was further elevated by ERRalpha knockdown, suggesting that activation of NF-kappaB signaling plays an important role in the deteriorative effects of ERRalpha knockdown on ALI."
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"LPS contamination in ouabain preparations could be responsible for NF-kappaB activation, but LPS was not detected in any samples using an assay sensitive to 1-10 pg/ml (XREF_SUPPLEMENTARY) and low doses of LPS (1 pg/ml) did not stimulate IkappaB-alpha degradation in our system (XREF_SUPPLEMENTARY)."
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"First, antecedent exposure of alveolar macrophages to S/R resulted in increased LPS induced IkappaBalpha degradation through activation of upstream signaling, an effect that resulted in increased NF-kappaB translocation and cytokine induced neutrophil chemoattractant gene expression."
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"Stimulation with hMRP8 or LPS caused IkappaBalpha degradation as represented by substantially reduced total IkappaBalpha protein and activated NF-kappaB p65 in naive cells; however, pre-stimulation with hMrp8 failed to prevent hMrp8- or LPS induced IkappaBalpha degradation (XREF_FIG) and NF-kappaB p65 phosphorylation (XREF_FIG)."
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"In the present study, we found LPS challenge induced the degradation of IkappaB-alpha and activation of NF-kappaB in vivo and in vitro, and the activation of NF-kappaB signaling was inhibited by DPQ treatment, suggesting that inhibition of NF-kappaB signaling plays a role in the protective effects of DPQ on ALI."
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"Pretreatment of rats with pyrrolidine dithiocarbamate (50, 100, and 200 mg/kg, i.p.), an inhibitor of NF-kappaB activation, prevented LPS induced I-kappaBalpha degradation and the resultant NF-kappaB activation and inhibited, in a dose related manner, the LPS induced CINC and ICAM-1 mRNA and protein expression."
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"Our research showed that LXA4 suppressed LPS induced proliferation, increased the proportion of the G0/G1 phase, decreased the proportion of the S phase, and downregulated the expression of Cyclin E. Besides these, LXA4 suppressed LPS induced IkappaBalpha degradation, NF-kappaB translocation, and the expression of IKK."
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"While GG6 reduced LPS induced IkappaB-alpha degradation and showed a trend towards reduced interleukin-1beta release, GG9 prevented the increase in proinflammatory CD80 + macrophage subset, downregulation of the anti-inflammatory CD206 + / CD163 + subset, increase in p38 phosphorylation, and increase in cell bound and secreted interleukin-1beta stimulated by LPS, at least in part through signalling pathways not involving Toll like receptor 4 and nuclear factor-kappaB."
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"Administration of RvD1 intravenously prior to LPS exposure significantly abrogated LPS induced inflammation, as indicated by histologic ALI score, and blunted elevations in BALF neutrophils, TNFalpha, and IL-6; RvD1 treatment also significantly inhibited LPS induced IkappaBalpha degradation, NF-kappaB p65 subunit nuclear translocation, and DNA binding activity of NF-kappaB."
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"The results showed that LPS stimulation caused degradation of IkappaB-alpha compared with negative control cells (P < 0.05), whereas PF-GPD blocked LPS induced degradation of IkappaB-alpha (P < 0.01), and inhibited NF-kappaB p65 translocation from the cytoplasm to the nucleus, thus interrupting the transcription and translation of inflammatory genes."