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IRF6 — TBCE

Text-mined interactions from Literome

Kiemer et al., Shock 2002 : ANP reduced TNFalpha release possibly by influencing post-translational processing of TNFalpha in LPS activated KCs
Jiang et al., Shock 2002 (Inflammation...) : The protein expression, phosphorylation, and activities of these MAPKs in LPS stimulated primary mouse KCs were determined with SDS-PAGE and western blotting using nonphosphorylated or phosphospecific antibodies or their corresponding substrates ... Although ERK1/2, p54JNK, and p38 kinases in LPS stimulated KCs have similar kinetics of activation, the activation of ERK1/2 and p38 kinases was the most prominent ... Inhibition of p38 MAPK with SB203580 inhibited the production of TNF-alpha and IL-10 by LPS stimulated KCs , whereas blockade of ERK1/2 with PD98059 could reduce TNF-alpha production, but did not affect IL-10 production ... These data indicate that LPS stimulation, although not inducing any change in protein expression, results in rapid activation of ERK1/2, p54JNK, and p38 kinases in KCs, and that they may have different importance in the regulation of pro- and anti-inflammatory responses by LPS stimulated KCs
Feng et al., Zhonghua Shao Shang Za Zhi 2002 : To explore the effect of LPS on the expression of CD14 and the activation of Kupffer cells (KCs)
Feng et al., Hepatobiliary Pancreat Dis Int 2003 : In rat KCs induced by LPS , the changes of CD14 and TLR4 expression were measured by RT-PCR and immunohistochemistry, and the expressions of TNF-alphamRNA, IL-6mRNA or the concentrations of TNF-alpha, IL-6 were estimated by in situ hybridization, radioimmunoassay, and others ... The expressions of CD14 and TLR4 in KCs induced by LPS were markedly increased in a dose dependent manner ( 10 mg/L-1 microg/L ) or in a time dependent manner ( 0.5 h-24 h ), with the peaked expression of CD14 at 3-6 hours ... There is a close relationship between LPS or the active mediators from KCs induced by LPS and the expressions of CD14, TLR4
Duryee et al., Alcohol Clin Exp Res 2004 : All three cytokines/chemokines were 3 to 5 times higher when SECs or KCs were stimulated by MAA-Alb in the presence of LPS , in contrast to cells stimulated with Alb or media in the presence of LPS
Shen et al., Life Sci 2005 : Leptin enhanced TNF-alpha production accompanied by a dose dependent increase of MAPK activity in lipopolysaccharide (LPS) stimulated KCs
Li et al., Am J Physiol Regul Integr Comp Physiol 2006 (Fever) : The animals were untreated or Kupffer cell ( KC ) depleted ; the essential involvement of KCs in LPS fever was shown previously
Liu et al., Zhonghua Wai Ke Za Zhi 2006 : The results indicated that prophylactic or simultaneous treatment with glycine could effectively inhibit LPS induced KCs activation by inhibiting IRAK-4 expression
Zhou et al., Chin J Cancer 2007 (Colonic Neoplasms) : This study was to investigate the effect of lipopolysaccharide (LPS) on antitumor activity of mouse KCs in vitro ... LPS may activate KCs in vitro, and enhance its antitumor activity as well
Liu et al., J Surg Res 2008 : Although a primary low dose of LPS stimulation obviously attenuated KCs response to the second LPS stimulation, the inhibitive influences were partly refracted in pIRAK-M-EP than in pCV-EP, indicating that the absence of IRAK-M caused abnormal enhancement of inflammatory effects
Xu et al., Am J Surg 2008 (Disease Models, Animal...) : Consistent with these in vivo experiments, enhanced secretion of IL-10 and inhibited expression of TLR4 and TNF-alpha caused by glycine pretreatment were also observed in LPS stimulated KCs
Wei et al., Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi 2011 : To study the role of glucocorticoid induced tumor necrosis factor related protein ligand ( GITRL ) on apoptosis of mouse Kupffer cells (KCs) induced by lipopolysaccharide (LPS)
Bankey et al., J Surg Res 1990 : Total protein phosphorylation was not significantly altered by LPS stimulation ; however, autoradiograms from PMA- and LPS stimulated KCs demonstrate enhanced phosphorylation of a 40-kDa protein ( 2.7 +/- 0.9-fold ) and a 33-kDa protein ( 3.1 +/- 1.0-fold ) which were inhibited by H-7