
IndraLab
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Lipopolysaccharide inhibits RELA. 109 / 109
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106
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"We therefore conclude that type I parasites do not inhibit TNF- or LPS stimulated NF-kappaB p65 translocation or TNF stimulated NF-kappaB-mediated transcription, but they may be able to modulate other pathways or host cell transcription factors which are important for expression of a small subset of TNF stimulated genes."
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"EF inhibited the LPS induced NF-kappaB p65 (LPS+EF 20mug/mL and 30mug/mL vs. LPS only : 0.78 +/-0.06 vs. 1.17 +/-0.08, P < 0.001; and 0.90 +/-0.06 vs. 1.17 +/-0.08, P = 0.002) and inhibitor of kappa B (IkappaBalpha) phosphorylation (LPS+EF 20mug/mL and 30mug/mL vs. LPS only : 0.25 +/-0.01 vs. 0.63 +/-0.03, P < 0.001; and 0.31 +/-0.01 vs. 0.63 +/-0.03, P < 0.001), LPS+EF 30mug/mL inhibited IkappaB kinase (IKKalpha and beta) phosphorylation (LPS+EF 30mug/mL vs. LPS only, 1.12 +/-0.14 vs. 1.71 +/-0.25, P = 0.002) in RAW 264.7 cells."
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"Co-incubation with MaR1 (10 nM) significantly attenuated LPS induced NF-kappaB p65 nuclear translocation in BMDMs [nuclear p65 + cells : 16 (3)%, P < 0.01 vs LPS group, XREF_FIG a and b], and partly reduced TNF-alpha levels in the culture medium [494 (49) pg ml -1, P = 0.01 vs LPS group; XREF_FIG c]."
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"This treatment pronouncedly alleviated LPS induced neuroinflammatory response, characterized by decreased 5LO, suppressed activation of microglia, decreased NF-kappaB p65, TNF-alpha and IL-1beta, and significantly increased the ratio of p-CREB and CREB or mBDNF and proBDNF in the hippocampus of the LPS challenged mice."
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"In fact, IkappaB kinase (IKK) assays showed that 1,25 (OH) 2 D 3 attenuated LPS induced IkappaBalpha phosphorylation in macrophages (XREF_FIG), which explains why 1,25 (OH) 2 D 3 stabilized IkappaBalpha protein reported previously, and immunostaining confirmed that 1,25 (OH) 2 D 3 blocked LPS induced p65 nuclear translocation RAW264.7 cells (XREF_FIG)."
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"These data suggest that HMGB1 and LPS stimulation could downregulate the expression NF-kappaB p65 in cytoplasmic proteins and increase the expression in nuclear proteins, thus leading to modulation of IL-1beta, IL-10, IFN-gamma, and TGF-beta expression; moreover, the suppressive function of Treg cells could be regulated by TLR4."