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lps tlr4 signaling (MedChemExpress)

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MedChemExpress lps tlr4 signaling
Lps Tlr4 Signaling, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 96/100, based on 31 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/lps+tlr4+signaling/pm42034314-68-15-9?v=MedChemExpress
Average 96 stars, based on 31 article reviews

lps tlr4 signaling - by Bioz Stars, 2026-07

96/100 stars

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Fig. 1 Effects of inhibition of Notch signaling on TLR4-mediated increases of CCL2 in DRG cell cultures. A NICD IF staining of the DRG cells treated with LPS (1 μg/mL) for 24 h. Scale bars, 50 μm. B-D Effects of inhibiting Notch signaling by DAPT (25 μM) on LPS-induced NICD (quantified as MFI and normalized to the control without LPS and DAPT treatment) (B), Ccl2 mRNA (C), and CCL2 protein (D) in cultured DRG cells (N = 4–8 cultures per treatment group). E–G Effects of inhibiting Notch signaling by sJag1 (40 μM) on LPS-increased NICD MFI (E), Ccl2 mRNA (F), and CCL2 protein (G) (N = 4–9 cultures per group)

Journal: Arthritis research & therapy

Article Title: Notch signaling is activated in knee-innervating dorsal root ganglia in experimental models of osteoarthritis joint pain.

doi: 10.1186/s13075-023-03039-1

Figure Lengend Snippet: Fig. 1 Effects of inhibition of Notch signaling on TLR4-mediated increases of CCL2 in DRG cell cultures. A NICD IF staining of the DRG cells treated with LPS (1 μg/mL) for 24 h. Scale bars, 50 μm. B-D Effects of inhibiting Notch signaling by DAPT (25 μM) on LPS-induced NICD (quantified as MFI and normalized to the control without LPS and DAPT treatment) (B), Ccl2 mRNA (C), and CCL2 protein (D) in cultured DRG cells (N = 4–8 cultures per treatment group). E–G Effects of inhibiting Notch signaling by sJag1 (40 μM) on LPS-increased NICD MFI (E), Ccl2 mRNA (F), and CCL2 protein (G) (N = 4–9 cultures per group)

Article Snippet: On day 4, TLR4 signaling was stimulated by adding lipopolysaccharide (LPS) (Catalog# tlrl-3pelps, InvivoGen, San Diego, CA) at a concentration of 1 μg/mL.

Techniques: Inhibition, Staining, Control, Cell Culture

Fig. 2 Effects of activation of Notch signaling on TLR4-mediated increases of CCL2 in DRG cell cultures. A NICD IF staining of DRG cells cultured with immobilized Jag1-Fc for 4 days. Representative images from each culture group are shown (N = 9 cultures per group). Scale bars, 50 μm. B-D Effects of activating Notch signaling with immobilized Jag1-Fc on LPS-induced NICD MFI (B), Ccl2 mRNA (C), and CCL2 protein (D) (N = 6–9 per group). The controls were immobilized with IgG-Fc

Journal: Arthritis research & therapy

Article Title: Notch signaling is activated in knee-innervating dorsal root ganglia in experimental models of osteoarthritis joint pain.

doi: 10.1186/s13075-023-03039-1

Figure Lengend Snippet: Fig. 2 Effects of activation of Notch signaling on TLR4-mediated increases of CCL2 in DRG cell cultures. A NICD IF staining of DRG cells cultured with immobilized Jag1-Fc for 4 days. Representative images from each culture group are shown (N = 9 cultures per group). Scale bars, 50 μm. B-D Effects of activating Notch signaling with immobilized Jag1-Fc on LPS-induced NICD MFI (B), Ccl2 mRNA (C), and CCL2 protein (D) (N = 6–9 per group). The controls were immobilized with IgG-Fc

Article Snippet: On day 4, TLR4 signaling was stimulated by adding lipopolysaccharide (LPS) (Catalog# tlrl-3pelps, InvivoGen, San Diego, CA) at a concentration of 1 μg/mL.

Techniques: Activation Assay, Staining, Cell Culture

Changes in viral titres on toll like receptor 4 activation with its specific ligand (LPS). A: mRNA expression of toll like receptor 4 (TLR4) is repressed in HepG2.2.15 cells compared to HepG2 cells. The mRNA expression of TLR4 in HepG2 cells was arbitrarily set as 1, and the fold change in HepG2.2.15 cells was then evaluated. ( a P < 0.05). HBV titre was evaluated in the culture supernatant of HepG2.2.15 cells after treatment with 1, 2 and 4 μg/mL of TLR4 ligand (LPS) for 72 h; B: HBV DNA was isolated from the culture media and the load was assessed by absolute real-time PCR using WHO standards. There was a dose dependent decrease in viral load ( a P < 0.05); C and D: HBsAg and HBeAg were detected from the culture supernatant of treated cells by ELISA. A dose-dependent repression of viral protein was observed ( a P < 0.05).

Journal: World Journal of Gastroenterology

Article Title: Anti-viral role of toll like receptor 4 in hepatitis B virus infection: An in vitro study

doi: 10.3748/wjg.v22.i47.10341

Figure Lengend Snippet: Changes in viral titres on toll like receptor 4 activation with its specific ligand (LPS). A: mRNA expression of toll like receptor 4 (TLR4) is repressed in HepG2.2.15 cells compared to HepG2 cells. The mRNA expression of TLR4 in HepG2 cells was arbitrarily set as 1, and the fold change in HepG2.2.15 cells was then evaluated. ( a P < 0.05). HBV titre was evaluated in the culture supernatant of HepG2.2.15 cells after treatment with 1, 2 and 4 μg/mL of TLR4 ligand (LPS) for 72 h; B: HBV DNA was isolated from the culture media and the load was assessed by absolute real-time PCR using WHO standards. There was a dose dependent decrease in viral load ( a P < 0.05); C and D: HBsAg and HBeAg were detected from the culture supernatant of treated cells by ELISA. A dose-dependent repression of viral protein was observed ( a P < 0.05).

Article Snippet: TLR4 signaling pathway was stimulated with its synthetic ligand LPS-B5 Ultrapure (Invivogen San Diego, CA, United States).

Techniques: Activation Assay, Expressing, Isolation, Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay

Modification in host cell cycle and expression of epigenetic signatures in HepG2.2.15 cells on toll like receptor 4 activation with its specific ligand (LPS). A: Flow cytometric analysis of HepG2.2.15 cells after treatment with LPS. Cell cycle analysis showing a partial release of G1/S arrest in treated cells compared to control HepG2.2.15 cells; B: Percentage distribution of cells in different phases of cell cycle showing even distribution of cells in G1 and S phase after LPS treatment; C: MTT assay showing cytotoxicity of LPS in HepG2.2.15 cells. No significant cell death was observed for the chosen concentration of the ligand at different time points; D: Status of epigenetic signatures in HepG2.2.15 cells after stimulation of toll like receptor 4 (TLR4). Protein expression of the methylation marks (H3K4Me3, H3K9Me3, H3K27Me3 and H3K36Me3) did not show significant change. Acetylation marks (H3K9Ac and H3K18Ac) showed an upregulated expression on triggering the cells with LPS ( a P < 0.05).

Journal: World Journal of Gastroenterology

Article Title: Anti-viral role of toll like receptor 4 in hepatitis B virus infection: An in vitro study

doi: 10.3748/wjg.v22.i47.10341

Figure Lengend Snippet: Modification in host cell cycle and expression of epigenetic signatures in HepG2.2.15 cells on toll like receptor 4 activation with its specific ligand (LPS). A: Flow cytometric analysis of HepG2.2.15 cells after treatment with LPS. Cell cycle analysis showing a partial release of G1/S arrest in treated cells compared to control HepG2.2.15 cells; B: Percentage distribution of cells in different phases of cell cycle showing even distribution of cells in G1 and S phase after LPS treatment; C: MTT assay showing cytotoxicity of LPS in HepG2.2.15 cells. No significant cell death was observed for the chosen concentration of the ligand at different time points; D: Status of epigenetic signatures in HepG2.2.15 cells after stimulation of toll like receptor 4 (TLR4). Protein expression of the methylation marks (H3K4Me3, H3K9Me3, H3K27Me3 and H3K36Me3) did not show significant change. Acetylation marks (H3K9Ac and H3K18Ac) showed an upregulated expression on triggering the cells with LPS ( a P < 0.05).

Article Snippet: TLR4 signaling pathway was stimulated with its synthetic ligand LPS-B5 Ultrapure (Invivogen San Diego, CA, United States).

Techniques: Modification, Expressing, Activation Assay, Cell Cycle Assay, Control, MTT Assay, Concentration Assay, Methylation

Changes in the expression of cell cycle regulators on toll like receptor 4 activation with its specific ligand (LPS) in HepG2.2.15 cells and p53 expression in liver biopsy samples from healthy and HBV-infected subjects. A: mRNA expression of the different cell cycle regulators (p53, p21, Rb, Cyclin D1, Cyclin E, Cyclin B1 and Cyclin A) on treating cells with LPS. mRNA expression of the mentioned genes of control HepG2.2.15 cells was arbitrarily set as 1 and the fold change of the treated cells was thereafter evaluated. p53, Rb and Cyclin D1 genes showed repressed mRNA expression in the treated cells. Cyclin E showed upregulated mRNA expression. p21, Cyclin B1 and Cyclin A did not show any significant change ( a P < 0.05); B: p53 mRNA expression of liver biopsy samples from CHB patients showed up-regulated expression compared to biopsy samples of control liver (with no history of HBV, HCV and HIV). mRNA expression of p53 in control liver was arbitrarily set as 1 and that in the CHB patients was then evaluated. p53 expression of CHB patients denoted as “HBV1”, “HBV2”, “HBV3”,”HBV4”, “HBV6” AND “HBV8” showed increased expression. TLR4: Toll like receptor 4.

Journal: World Journal of Gastroenterology

Article Title: Anti-viral role of toll like receptor 4 in hepatitis B virus infection: An in vitro study

doi: 10.3748/wjg.v22.i47.10341

Figure Lengend Snippet: Changes in the expression of cell cycle regulators on toll like receptor 4 activation with its specific ligand (LPS) in HepG2.2.15 cells and p53 expression in liver biopsy samples from healthy and HBV-infected subjects. A: mRNA expression of the different cell cycle regulators (p53, p21, Rb, Cyclin D1, Cyclin E, Cyclin B1 and Cyclin A) on treating cells with LPS. mRNA expression of the mentioned genes of control HepG2.2.15 cells was arbitrarily set as 1 and the fold change of the treated cells was thereafter evaluated. p53, Rb and Cyclin D1 genes showed repressed mRNA expression in the treated cells. Cyclin E showed upregulated mRNA expression. p21, Cyclin B1 and Cyclin A did not show any significant change ( a P < 0.05); B: p53 mRNA expression of liver biopsy samples from CHB patients showed up-regulated expression compared to biopsy samples of control liver (with no history of HBV, HCV and HIV). mRNA expression of p53 in control liver was arbitrarily set as 1 and that in the CHB patients was then evaluated. p53 expression of CHB patients denoted as “HBV1”, “HBV2”, “HBV3”,”HBV4”, “HBV6” AND “HBV8” showed increased expression. TLR4: Toll like receptor 4.

Article Snippet: TLR4 signaling pathway was stimulated with its synthetic ligand LPS-B5 Ultrapure (Invivogen San Diego, CA, United States).

Techniques: Expressing, Activation Assay, Infection, Control

Changes in expression of important toll like receptor 4 pathway signaling molecules and pro-inflammatory cytokines on toll like receptor 4 activation with its specific ligand (LPS). A: Toll like receptor 4 (TLR4) pathway was stimulated with its specific ligand LPS-B5 Ultrapure. At the specified dose, the signaling molecules involved in TLR4 signaling pathway showed upregulated mRNA expression compared to HepG2.2.15 cells ( a P < 0.05); B: Cytokine concentration on triggering the TLR4 pathway. Pro-inflammatory cytokines (IL-1B, IL-10, IL-12p70 and TNF-A) showed increased protein expression on TLR4 activation by using cytokine bead array.

Journal: World Journal of Gastroenterology

Article Title: Anti-viral role of toll like receptor 4 in hepatitis B virus infection: An in vitro study

doi: 10.3748/wjg.v22.i47.10341

Figure Lengend Snippet: Changes in expression of important toll like receptor 4 pathway signaling molecules and pro-inflammatory cytokines on toll like receptor 4 activation with its specific ligand (LPS). A: Toll like receptor 4 (TLR4) pathway was stimulated with its specific ligand LPS-B5 Ultrapure. At the specified dose, the signaling molecules involved in TLR4 signaling pathway showed upregulated mRNA expression compared to HepG2.2.15 cells ( a P < 0.05); B: Cytokine concentration on triggering the TLR4 pathway. Pro-inflammatory cytokines (IL-1B, IL-10, IL-12p70 and TNF-A) showed increased protein expression on TLR4 activation by using cytokine bead array.

Article Snippet: TLR4 signaling pathway was stimulated with its synthetic ligand LPS-B5 Ultrapure (Invivogen San Diego, CA, United States).

Techniques: Expressing, Activation Assay, Concentration Assay

Changes in protein expression and nuclear translocation of nuclear factor-κB on triggering HepG2.2.15 cells with toll like receptor 4 specific ligand, LPS. A: Protein expression of p53 and nuclear factor-κB (NF-κB) in HepG2.2.15 cells and LPS- treated HepG2.2.15 cells. β-actin was considered as control. Quantitative analysis showed that p53 and NF-κB protein expression was repressed and upregulated respectively in treated cells; B: Confocal imaging showing nuclear uptake of NF-κB p65 subunit from cytoplasm in cells where HepG2.2.15 cells are taken as control and HepG2.2.15 cells stimulated with toll like receptor 4 (TLR4) ligand, LPS. NF-κB concentration was higher in the nucleus of LPS-treated cells compared to control cells.

Journal: World Journal of Gastroenterology

Article Title: Anti-viral role of toll like receptor 4 in hepatitis B virus infection: An in vitro study

doi: 10.3748/wjg.v22.i47.10341

Figure Lengend Snippet: Changes in protein expression and nuclear translocation of nuclear factor-κB on triggering HepG2.2.15 cells with toll like receptor 4 specific ligand, LPS. A: Protein expression of p53 and nuclear factor-κB (NF-κB) in HepG2.2.15 cells and LPS- treated HepG2.2.15 cells. β-actin was considered as control. Quantitative analysis showed that p53 and NF-κB protein expression was repressed and upregulated respectively in treated cells; B: Confocal imaging showing nuclear uptake of NF-κB p65 subunit from cytoplasm in cells where HepG2.2.15 cells are taken as control and HepG2.2.15 cells stimulated with toll like receptor 4 (TLR4) ligand, LPS. NF-κB concentration was higher in the nucleus of LPS-treated cells compared to control cells.

Article Snippet: TLR4 signaling pathway was stimulated with its synthetic ligand LPS-B5 Ultrapure (Invivogen San Diego, CA, United States).

Techniques: Expressing, Translocation Assay, Control, Imaging, Concentration Assay

Recruitment of relevant downstream regulator inhibitors in toll like receptor 4 signaling to identify the pathway responsible for its anti-viral action. A: Pictorial representation of toll like receptor 4 (TLR4) signaling pathway and the important inhibitors of signaling molecules have been highlighted; B: HBV DNA was evaluated in the supernatant from cells pre-treated with LPS, singly or in conjunction with the inhibitors. Anti-viral action of TLR4 was abolished on blocking the TLR4 pathway with PDTC (NF-κB inhibitor) ( a P < 0.05); C, D: Viral proteins (HBsAg and HBeAg) showed highest concentration on using PDTC. The antiviral action of TLR4 is probably operated through NF-κB pathway ( a P < 0.05).

Journal: World Journal of Gastroenterology

Article Title: Anti-viral role of toll like receptor 4 in hepatitis B virus infection: An in vitro study

doi: 10.3748/wjg.v22.i47.10341

Figure Lengend Snippet: Recruitment of relevant downstream regulator inhibitors in toll like receptor 4 signaling to identify the pathway responsible for its anti-viral action. A: Pictorial representation of toll like receptor 4 (TLR4) signaling pathway and the important inhibitors of signaling molecules have been highlighted; B: HBV DNA was evaluated in the supernatant from cells pre-treated with LPS, singly or in conjunction with the inhibitors. Anti-viral action of TLR4 was abolished on blocking the TLR4 pathway with PDTC (NF-κB inhibitor) ( a P < 0.05); C, D: Viral proteins (HBsAg and HBeAg) showed highest concentration on using PDTC. The antiviral action of TLR4 is probably operated through NF-κB pathway ( a P < 0.05).

Article Snippet: TLR4 signaling pathway was stimulated with its synthetic ligand LPS-B5 Ultrapure (Invivogen San Diego, CA, United States).

Techniques: Blocking Assay, Concentration Assay

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