| Name | Toll like receptor 4 |
|---|---|
| Synonyms | CD284; CD284 antigen; TLR 4; TLR4; TOLL; Toll like receptor 4; Toll like receptor 4 precursor; hToll… |
| Name | cycloheximide |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 15563689 | Zhou X, Gao XP, Fan J, Liu Q, Anwar KN, Frey RS, Malik AB: LPS activation of Toll-like receptor 4 signals CD11b/CD18 expression in neutrophils. Am J Physiol Lung Cell Mol Physiol. 2005 Apr;288(4):L655-62. Epub 2004 Nov 24. TLR4-activated CD11b expression was cycloheximide sensitive and involved the activation of transcription factors, NF-kappaB and c-Jun/PU.1. |
86(1,1,1,6) | Details |
| 17304101 | Pearl-Yafe M, Fabian I, Halperin D, Flatau E, Werber S, Shalit I: Interferon-gamma and bacterial lipopolysaccharide act synergistically on human neutrophils enhancing interleukin-8, interleukin-1beta, tumor necrosis factor-alpha, and interleukin-12 p70 secretion and phagocytosis via upregulation of toll-like receptor 4. Shock. 2007 Mar;27(3):226-31. Using the protein synthesis inhibitor cycloheximide and measuring the expression of CD35 in neutrophils stimulated with IFN-gamma and LPS alone or in combination, we could demonstrate that IFN-gamma enhances TLR4 by de novo protein synthesis, whereas the addition of LPS acts synergistically by enhancing vesicular mobilization to the cell surface. |
34(0,1,1,4) | Details |
| 18422969 | Necela BM, Su W, Thompson EA: Toll-like receptor 4 mediates cross-talk between peroxisome proliferator-activated receptor gamma and nuclear factor-kappaB in macrophages. Immunology. 2008 Nov;125(3):344-58. Epub 2008 Apr 18. Inhibition of PPARgamma expression was not blocked by cycloheximide, indicating that de novo protein synthesis is not required for LPS-mediated suppression of PPARgamma. |
4(0,0,0,4) | Details |
| 18854426 | Gu JQ, Ikuyama S, Wei P, Fan B, Oyama J, Inoguchi T, Nishimura J: Pycnogenol, an extract from French maritime pine, suppresses Toll-like receptor 4-mediated expression of adipose differentiation-related protein in macrophages. Am J Physiol Endocrinol Metab. 2008 Dec;295(6):E1390-400. Epub 2008 Oct 14. Actinomycin D almost completely abolished the LPS effect, whereas cycloheximide decreased the expression at 12 h, indicating that the LPS-induced ADRP expression was stimulated at the transcriptional level and was also mediated by new protein synthesis. |
4(0,0,0,4) | Details |
| 16690986 | Lee KY, Ho SC, Lin HC, Lin SM, Liu CY, Huang CD, Wang CH, Chung KF, Kuo HP: Neutrophil-derived elastase induces TGF-beta1 secretion in human airway smooth muscle via NF-kappaB pathway. Am J Respir Cell Mol Biol. 2006 Oct;35(4):407-14. Epub 2006 May 11. This induction was inhibited by actinomycin D (5 mM), cycloheximide (5 mM), and NF-kappaB inhibitors, including pyrrolidine dithiocarbamate (PDTC, 1 mM), (2.5 mM), and salyicylate (2.5 mM). Association of IL-1 receptor-associated kinase (IRAK) with MyD88 was studied by co-immunoprecipitation and Toll-like receptor 4 (TLR4) determined by FACS scan and Western blotting. |
3(0,0,0,3) | Details |
| 16464966 | Balzary RW, Cocks TM: Lipopolysaccharide induces epithelium- and (2)-dependent relaxation of mouse isolated trachea through activation of cyclooxygenase (COX)-1 and COX-2. J Pharmacol Exp Ther. 2006 May;317(2):806-12. Epub 2006 Feb 7. Lipopolysaccharide (LPS), a Toll-like receptor (TLR) 4 agonist, causes airway hyperreactivity through nuclear factor-kappaB (NF-kappaB). The LPS antagonist polymixin B; the nonselective COX inhibitor indomethacin; the selective COX-1 and COX-2 inhibitors 5-(4-chlorophenyl)-1-(4-methoxyphenyl)-3-(trifluoromethyl)-1H-pyrazole (SC560) and 4-[5-(4-chlorophenyl)-1-(trifluoromethyl)-1H-pyrazol-1-yl]-benzenesulfonam ide (SC236), respectively; the transcription inhibitor actinomycin D; the translation inhibitor cycloheximide; the p38 mitogen-activated protein kinase (p38 MAPK) inhibitor 4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)-1H-imadazole (SB203580); and a combination of the mixed DP/EP1/EP2 receptor antagonist 6-isopropoxy-9-xanthone-2-carboxylic acid (AH6809) and the EP4 receptor antagonist 4'-[3-butyl-5-oxo-1-(2-trifluoromethyl-phenyl)-1-5-dihydro-[1,2,4] triazol- 4-ylmethyl]-biphenyl-2- (3-methyl-thiophene-2-carbonyl)-amide (L-161982) all abolished relaxation to LPS, giving instead slowly developing, small contractions over 60 min. |
3(0,0,0,3) | Details |
| 16166516 | Covert MW, Leung TH, Gaston JE, Baltimore D: Achieving stability of lipopolysaccharide-induced NF-kappaB activation. Science. 2005 Sep 16;309(5742):1854-7. LPS binding to Toll-like receptor 4 (TLR4) causes activation of NF-kappaB that requires two downstream pathways, each of which when isolated exhibits damped oscillatory behavior. |
2(0,0,0,2) | Details |
| 16790802 | Bennouna S, Sukhumavasi W, Denkers EY: Toxoplasma gondii inhibits toll-like receptor 4 ligand-induced mobilization of intracellular tumor necrosis factor alpha to the surface of mouse peritoneal neutrophils. Infect Immun. 2006 Jul;74(7):4274-81. In contrast to intermediate inhibitory effects in nontreated neutrophils, T. gondii induced a complete blockade in LPS-induced surface TNF-alpha expression in the presence of the protein synthesis inhibitor cycloheximide. |
1(0,0,0,1) | Details |
| 16236128 | Ding A, Yu H, Yang J, Shi S, Ehrt S: Induction of macrophage-derived SLPI by Mycobacterium tuberculosis depends on TLR2 but not MyD88. Immunology. 2005 Nov;116(3):381-9. HK-Mtb-induced SLPI mRNA expression was sensitive neither to a protein synthesis inhibitor, cycloheximide, nor to an actin polymerization blocker, cytochalasin D. Macrophages from Toll-like receptor 4 (TLR4)-/- or MyD88-/- mice responded to M. tuberculosis similarly to wild-type macrophages by exhibiting increased SLPI expression. |
1(0,0,0,1) | Details |
| 15749881 | Monari C, Pericolini E, Bistoni G, Casadevall A, Kozel TR, Vecchiarelli A: Cryptococcus neoformans capsular glucuronoxylomannan induces expression of fas ligand in macrophages. J Immunol. 2005 Mar 15;174(6):3461-8. The results reported here show that 1) soluble purified GXM induces a long-lasting, and potent up-regulation of Fas ligand (FasL) on macrophages, 2) the up-regulation of FasL is related to induced synthesis and increased mobilization to the cellular surface, 3) this effect is largely mediated by interaction between GXM and TLR4, 4) FasL up-regulation occurs exclusively in GXM-loaded macrophages, 5) macrophages that show up-regulation of FasL induce apoptosis of activated T cells expressing Fas and Jurkat cells that constitutively express Fas, and 6) anti-Fas Abs rescue T cells from apoptosis induced by GXM. |
1(0,0,0,1) | Details |
| 16237104 | Mandal P, Novotny M, Hamilton TA: Lipopolysaccharide induces formyl peptide receptor 1 gene expression in macrophages and neutrophils via transcriptional and posttranscriptional mechanisms. J Immunol. 2005 Nov 1;175(9):6085-91. First, the response to LPS is partially blocked by the translational inhibitor cycloheximide. Furthermore, supernatants from LPS-treated wild-type macrophages can stimulate FPR1 mRNA expression in LPS-insensitive macrophages from TLR4-mutant mice. |
1(0,0,0,1) | Details |
| 15626483 | Fischer SF, Rehm M, Bauer A, Hofling F, Kirschnek S, Rutz M, Bauer S, Wagner H, Hacker G: Toll-like receptor 9 signaling can sensitize fibroblasts for apoptosis. Immunol Lett. 2005 Feb 15;97(1):115-22. CpG-DNA-induced apoptosis was reduced by cycloheximide suggesting that de novo protein synthesis was required. |
0(0,0,0,0) | Details |
| 16525587 | Zacharowski K, Sucker C, Zacharowski P, Hartmann M: Thrombelastography for the monitoring of lipopolysaccharide induced activation of coagulation. Thromb Haemost. 2006 Mar;95(3):557-61. Experiments with the protein synthesis inhibitor cycloheximide and active site-inhibited factor VIIa revealed that LPS exerts its effects via the synthesis of tissue factor. |
0(0,0,0,0) | Details |
| 19439685 | Hartmann M, Ozlugedik S, Peters J: Thiopental inhibits lipopolysaccharide-induced tissue factor expression. Anesth Analg. 2009 Jul;109(1):109-13. Epub 2009 May 13. After recalcification, clotting time (CT) was determined by rotational thrombelastometry. (ii) The mechanism of the LPS-induced shortening of CT was investigated using the tissue factor blocker active-site inhibited factor VIIa and the protein synthesis inhibitor cycloheximide. (iii) A concentration response curve for the effect of tissue factor on CT was generated. |
0(0,0,0,0) | Details |