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anti human cd284 tlr4  (Revvity)


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    Structured Review

    Revvity anti human cd284 tlr4
    Primer sequences used for reverse transcription-quantitative PCR analysis.
    Anti Human Cd284 Tlr4, supplied by Revvity, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti human cd284 tlr4/product/Revvity
    Average 86 stars, based on 1 article reviews
    anti human cd284 tlr4 - by Bioz Stars, 2025-07
    86/100 stars

    Images

    1) Product Images from "Understanding the role of iron/heme metabolism in the anti‑inflammatory effects of natural sulfur molecules against lipopolysaccharide‑induced inflammation"

    Article Title: Understanding the role of iron/heme metabolism in the anti‑inflammatory effects of natural sulfur molecules against lipopolysaccharide‑induced inflammation

    Journal: Molecular Medicine Reports

    doi: 10.3892/mmr.2025.13542

    Primer sequences used for reverse transcription-quantitative PCR analysis.
    Figure Legend Snippet: Primer sequences used for reverse transcription-quantitative PCR analysis.

    Techniques Used: Sequencing

    Sulfur compounds inhibit LPS-induced TLR expression. (A) Western blot analysis of TLR2 and TLR4 expression in THP-1 cells treated with LPS (10 ng/ml) + NTS (3 µg/ml), MSM (200 mM) or TLR-C34 (40 µM) for 48 h. (B) Reverse transcription-quantitative PCR analysis of the relative expression levels of TLR2 and TLR4 normalized to GAPDH following treatment with LPS (10 ng/ml) + NTS (3 µg/ml), MSM (200 mM) or TLR-C34 (40 µM) for 48 h. ***P<0.001; # P<0.001 vs. non-treated control (one-way ANOVA and Tukey's test). (C) Flow cytometry showing the inhibition of LPS-induced TLR4 expression by 48-h treatment with NTS (3 µg/ml), MSM (200 mM) and TLR-C34 (40 µM). LPS, lipopolysaccharide; MSM, methylsulfonylmethane; NTS, nontoxic sulfur; TLR, Toll-like receptor.
    Figure Legend Snippet: Sulfur compounds inhibit LPS-induced TLR expression. (A) Western blot analysis of TLR2 and TLR4 expression in THP-1 cells treated with LPS (10 ng/ml) + NTS (3 µg/ml), MSM (200 mM) or TLR-C34 (40 µM) for 48 h. (B) Reverse transcription-quantitative PCR analysis of the relative expression levels of TLR2 and TLR4 normalized to GAPDH following treatment with LPS (10 ng/ml) + NTS (3 µg/ml), MSM (200 mM) or TLR-C34 (40 µM) for 48 h. ***P<0.001; # P<0.001 vs. non-treated control (one-way ANOVA and Tukey's test). (C) Flow cytometry showing the inhibition of LPS-induced TLR4 expression by 48-h treatment with NTS (3 µg/ml), MSM (200 mM) and TLR-C34 (40 µM). LPS, lipopolysaccharide; MSM, methylsulfonylmethane; NTS, nontoxic sulfur; TLR, Toll-like receptor.

    Techniques Used: Expressing, Western Blot, Reverse Transcription, Real-time Polymerase Chain Reaction, Control, Flow Cytometry, Inhibition

    Sulfur compounds induce DNA damage response following LPS-induced DNA damage. (A) Images of the comet assay were captured by fluorescence microscopy at ×10 and ×40 magnification levels, showing the fragmented DNA migrating out of the nucleoid body, which formed a comet tail following treatment with LPS (10 ng/ml) + NTS (3 µg/ml), MSM (200 mM) or TLR-C34 (40 µM) for 48 h. *P<0.05 and ***P<0.001; $ P<0.05 vs. non-treated control; and $$$ P<0.001 vs. non-treated control (one-way ANOVA and Tukey's test). (B) Western blot analysis of THP-1 cells; NTS (3 µg/ml) and MSM (200 mM) inhibited the LPS-induced expression of p-ATM, p-ATR, p-Chk2, p-BRCA1, and p-p53. However, the expression levels of p-MDM2 were suppressed by LPS treatment, and were increased by NTS (3 µg/ml), MSM (200 mM) or TLR4-C34 (40 µM). LPS, lipopolysaccharide; MSM, methylsulfonylmethane; NTS, nontoxic sulfur; p-, phosphorylated; TLR, Toll-like receptor.
    Figure Legend Snippet: Sulfur compounds induce DNA damage response following LPS-induced DNA damage. (A) Images of the comet assay were captured by fluorescence microscopy at ×10 and ×40 magnification levels, showing the fragmented DNA migrating out of the nucleoid body, which formed a comet tail following treatment with LPS (10 ng/ml) + NTS (3 µg/ml), MSM (200 mM) or TLR-C34 (40 µM) for 48 h. *P<0.05 and ***P<0.001; $ P<0.05 vs. non-treated control; and $$$ P<0.001 vs. non-treated control (one-way ANOVA and Tukey's test). (B) Western blot analysis of THP-1 cells; NTS (3 µg/ml) and MSM (200 mM) inhibited the LPS-induced expression of p-ATM, p-ATR, p-Chk2, p-BRCA1, and p-p53. However, the expression levels of p-MDM2 were suppressed by LPS treatment, and were increased by NTS (3 µg/ml), MSM (200 mM) or TLR4-C34 (40 µM). LPS, lipopolysaccharide; MSM, methylsulfonylmethane; NTS, nontoxic sulfur; p-, phosphorylated; TLR, Toll-like receptor.

    Techniques Used: Single Cell Gel Electrophoresis, Fluorescence, Microscopy, Control, Western Blot, Expressing

    Molecular mechanism of LPS-induced regulation of the inflammatory response through iron/heme metabolism and TLR4/NF-κB expression through the canonical NF-κB and PKC-mediated inflammatory pathways. The anti-inflammatory activities of NTS and MSM were achieved by inhibiting iron/heme metabolism and suppressing the expression of TLR4/NF-κB signaling molecules, thus blocking the binding of NF-κB to the gene promoters of proinflammatory cytokines. DMT1, divalent metal transporter 1; Fe 2+ , ferrous ion; FPN, ferroportin; TfR, transferrin receptor; TLR4, Toll-like receptor 4.
    Figure Legend Snippet: Molecular mechanism of LPS-induced regulation of the inflammatory response through iron/heme metabolism and TLR4/NF-κB expression through the canonical NF-κB and PKC-mediated inflammatory pathways. The anti-inflammatory activities of NTS and MSM were achieved by inhibiting iron/heme metabolism and suppressing the expression of TLR4/NF-κB signaling molecules, thus blocking the binding of NF-κB to the gene promoters of proinflammatory cytokines. DMT1, divalent metal transporter 1; Fe 2+ , ferrous ion; FPN, ferroportin; TfR, transferrin receptor; TLR4, Toll-like receptor 4.

    Techniques Used: Expressing, Blocking Assay, Binding Assay



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    Primer sequences used for reverse transcription-quantitative PCR analysis.

    Journal: Molecular Medicine Reports

    Article Title: Understanding the role of iron/heme metabolism in the anti‑inflammatory effects of natural sulfur molecules against lipopolysaccharide‑induced inflammation

    doi: 10.3892/mmr.2025.13542

    Figure Lengend Snippet: Primer sequences used for reverse transcription-quantitative PCR analysis.

    Article Snippet: After cultured cells were washed with pre-chilled PBS, cell pellets were incubated with 10% BSA (cat. no. A3311; MilliporeSigma) on ice for 20 min. PE-conjugated anti-human CD284 (TLR4) antibody (1:200; cat. no. 312806; Biolegend, Inc.) and APC-conjugated anti-human CD282 (TLR2) antibody (1:200; cat. no. 309720; Biolegend, Inc.) was used to stain the cells on ice for 30 min. Stained cells were then washed with pre-chilled PBS.

    Techniques: Sequencing

    Sulfur compounds inhibit LPS-induced TLR expression. (A) Western blot analysis of TLR2 and TLR4 expression in THP-1 cells treated with LPS (10 ng/ml) + NTS (3 µg/ml), MSM (200 mM) or TLR-C34 (40 µM) for 48 h. (B) Reverse transcription-quantitative PCR analysis of the relative expression levels of TLR2 and TLR4 normalized to GAPDH following treatment with LPS (10 ng/ml) + NTS (3 µg/ml), MSM (200 mM) or TLR-C34 (40 µM) for 48 h. ***P<0.001; # P<0.001 vs. non-treated control (one-way ANOVA and Tukey's test). (C) Flow cytometry showing the inhibition of LPS-induced TLR4 expression by 48-h treatment with NTS (3 µg/ml), MSM (200 mM) and TLR-C34 (40 µM). LPS, lipopolysaccharide; MSM, methylsulfonylmethane; NTS, nontoxic sulfur; TLR, Toll-like receptor.

    Journal: Molecular Medicine Reports

    Article Title: Understanding the role of iron/heme metabolism in the anti‑inflammatory effects of natural sulfur molecules against lipopolysaccharide‑induced inflammation

    doi: 10.3892/mmr.2025.13542

    Figure Lengend Snippet: Sulfur compounds inhibit LPS-induced TLR expression. (A) Western blot analysis of TLR2 and TLR4 expression in THP-1 cells treated with LPS (10 ng/ml) + NTS (3 µg/ml), MSM (200 mM) or TLR-C34 (40 µM) for 48 h. (B) Reverse transcription-quantitative PCR analysis of the relative expression levels of TLR2 and TLR4 normalized to GAPDH following treatment with LPS (10 ng/ml) + NTS (3 µg/ml), MSM (200 mM) or TLR-C34 (40 µM) for 48 h. ***P<0.001; # P<0.001 vs. non-treated control (one-way ANOVA and Tukey's test). (C) Flow cytometry showing the inhibition of LPS-induced TLR4 expression by 48-h treatment with NTS (3 µg/ml), MSM (200 mM) and TLR-C34 (40 µM). LPS, lipopolysaccharide; MSM, methylsulfonylmethane; NTS, nontoxic sulfur; TLR, Toll-like receptor.

    Article Snippet: After cultured cells were washed with pre-chilled PBS, cell pellets were incubated with 10% BSA (cat. no. A3311; MilliporeSigma) on ice for 20 min. PE-conjugated anti-human CD284 (TLR4) antibody (1:200; cat. no. 312806; Biolegend, Inc.) and APC-conjugated anti-human CD282 (TLR2) antibody (1:200; cat. no. 309720; Biolegend, Inc.) was used to stain the cells on ice for 30 min. Stained cells were then washed with pre-chilled PBS.

    Techniques: Expressing, Western Blot, Reverse Transcription, Real-time Polymerase Chain Reaction, Control, Flow Cytometry, Inhibition

    Sulfur compounds induce DNA damage response following LPS-induced DNA damage. (A) Images of the comet assay were captured by fluorescence microscopy at ×10 and ×40 magnification levels, showing the fragmented DNA migrating out of the nucleoid body, which formed a comet tail following treatment with LPS (10 ng/ml) + NTS (3 µg/ml), MSM (200 mM) or TLR-C34 (40 µM) for 48 h. *P<0.05 and ***P<0.001; $ P<0.05 vs. non-treated control; and $$$ P<0.001 vs. non-treated control (one-way ANOVA and Tukey's test). (B) Western blot analysis of THP-1 cells; NTS (3 µg/ml) and MSM (200 mM) inhibited the LPS-induced expression of p-ATM, p-ATR, p-Chk2, p-BRCA1, and p-p53. However, the expression levels of p-MDM2 were suppressed by LPS treatment, and were increased by NTS (3 µg/ml), MSM (200 mM) or TLR4-C34 (40 µM). LPS, lipopolysaccharide; MSM, methylsulfonylmethane; NTS, nontoxic sulfur; p-, phosphorylated; TLR, Toll-like receptor.

    Journal: Molecular Medicine Reports

    Article Title: Understanding the role of iron/heme metabolism in the anti‑inflammatory effects of natural sulfur molecules against lipopolysaccharide‑induced inflammation

    doi: 10.3892/mmr.2025.13542

    Figure Lengend Snippet: Sulfur compounds induce DNA damage response following LPS-induced DNA damage. (A) Images of the comet assay were captured by fluorescence microscopy at ×10 and ×40 magnification levels, showing the fragmented DNA migrating out of the nucleoid body, which formed a comet tail following treatment with LPS (10 ng/ml) + NTS (3 µg/ml), MSM (200 mM) or TLR-C34 (40 µM) for 48 h. *P<0.05 and ***P<0.001; $ P<0.05 vs. non-treated control; and $$$ P<0.001 vs. non-treated control (one-way ANOVA and Tukey's test). (B) Western blot analysis of THP-1 cells; NTS (3 µg/ml) and MSM (200 mM) inhibited the LPS-induced expression of p-ATM, p-ATR, p-Chk2, p-BRCA1, and p-p53. However, the expression levels of p-MDM2 were suppressed by LPS treatment, and were increased by NTS (3 µg/ml), MSM (200 mM) or TLR4-C34 (40 µM). LPS, lipopolysaccharide; MSM, methylsulfonylmethane; NTS, nontoxic sulfur; p-, phosphorylated; TLR, Toll-like receptor.

    Article Snippet: After cultured cells were washed with pre-chilled PBS, cell pellets were incubated with 10% BSA (cat. no. A3311; MilliporeSigma) on ice for 20 min. PE-conjugated anti-human CD284 (TLR4) antibody (1:200; cat. no. 312806; Biolegend, Inc.) and APC-conjugated anti-human CD282 (TLR2) antibody (1:200; cat. no. 309720; Biolegend, Inc.) was used to stain the cells on ice for 30 min. Stained cells were then washed with pre-chilled PBS.

    Techniques: Single Cell Gel Electrophoresis, Fluorescence, Microscopy, Control, Western Blot, Expressing

    Molecular mechanism of LPS-induced regulation of the inflammatory response through iron/heme metabolism and TLR4/NF-κB expression through the canonical NF-κB and PKC-mediated inflammatory pathways. The anti-inflammatory activities of NTS and MSM were achieved by inhibiting iron/heme metabolism and suppressing the expression of TLR4/NF-κB signaling molecules, thus blocking the binding of NF-κB to the gene promoters of proinflammatory cytokines. DMT1, divalent metal transporter 1; Fe 2+ , ferrous ion; FPN, ferroportin; TfR, transferrin receptor; TLR4, Toll-like receptor 4.

    Journal: Molecular Medicine Reports

    Article Title: Understanding the role of iron/heme metabolism in the anti‑inflammatory effects of natural sulfur molecules against lipopolysaccharide‑induced inflammation

    doi: 10.3892/mmr.2025.13542

    Figure Lengend Snippet: Molecular mechanism of LPS-induced regulation of the inflammatory response through iron/heme metabolism and TLR4/NF-κB expression through the canonical NF-κB and PKC-mediated inflammatory pathways. The anti-inflammatory activities of NTS and MSM were achieved by inhibiting iron/heme metabolism and suppressing the expression of TLR4/NF-κB signaling molecules, thus blocking the binding of NF-κB to the gene promoters of proinflammatory cytokines. DMT1, divalent metal transporter 1; Fe 2+ , ferrous ion; FPN, ferroportin; TfR, transferrin receptor; TLR4, Toll-like receptor 4.

    Article Snippet: After cultured cells were washed with pre-chilled PBS, cell pellets were incubated with 10% BSA (cat. no. A3311; MilliporeSigma) on ice for 20 min. PE-conjugated anti-human CD284 (TLR4) antibody (1:200; cat. no. 312806; Biolegend, Inc.) and APC-conjugated anti-human CD282 (TLR2) antibody (1:200; cat. no. 309720; Biolegend, Inc.) was used to stain the cells on ice for 30 min. Stained cells were then washed with pre-chilled PBS.

    Techniques: Expressing, Blocking Assay, Binding Assay

    The percentage of the neutrophil extracellular trap (NET) area in the SS and FS plots of flow cytometry was compared among untreated neutrophils and samples following NET induction with E. coli DH5α or PMA. (a) Expression intensities of Cit-H3, flavocytochrome b558, SYTOX™ Green, CD14, TLR2, TLR4, and LL-37 were compared between untreated neutrophil and NET areas after E. coli DH5α stimulation. (b) NET ratios were compared among untreated neutrophils and samples treated with E. coli DH5α or PMA using enzyme-linked immunosorbent assay (ELISA). Data are presented as mean ± standard deviation (SD) (n = 3). Statistical analysis was performed using one-way analysis of variance (ANOVA) followed by Dunnett’s test. ** p < 0.01. (c) Western blotting was performed to examine CD14 and Cit-H3 protein levels in untreated neutrophils and those stimulated with E. coli DH5α or PMA. Band intensities were quantified using ImageJ and normalized to β-actin. Data are presented as mean ± standard deviation (SD) (n = 3). Data are presented as mean ± SD (n = 3). Statistical analysis was performed using one-way ANOVA followed by Tukey–Kramer’s HSD test. ** p < 0.01

    Journal: bioRxiv

    Article Title: Proteinase 3 is involved in presepsin production through neutrophil extracellular trap phagocytosis by macrophages

    doi: 10.1101/2025.05.02.651854

    Figure Lengend Snippet: The percentage of the neutrophil extracellular trap (NET) area in the SS and FS plots of flow cytometry was compared among untreated neutrophils and samples following NET induction with E. coli DH5α or PMA. (a) Expression intensities of Cit-H3, flavocytochrome b558, SYTOX™ Green, CD14, TLR2, TLR4, and LL-37 were compared between untreated neutrophil and NET areas after E. coli DH5α stimulation. (b) NET ratios were compared among untreated neutrophils and samples treated with E. coli DH5α or PMA using enzyme-linked immunosorbent assay (ELISA). Data are presented as mean ± standard deviation (SD) (n = 3). Statistical analysis was performed using one-way analysis of variance (ANOVA) followed by Dunnett’s test. ** p < 0.01. (c) Western blotting was performed to examine CD14 and Cit-H3 protein levels in untreated neutrophils and those stimulated with E. coli DH5α or PMA. Band intensities were quantified using ImageJ and normalized to β-actin. Data are presented as mean ± standard deviation (SD) (n = 3). Data are presented as mean ± SD (n = 3). Statistical analysis was performed using one-way ANOVA followed by Tukey–Kramer’s HSD test. ** p < 0.01

    Article Snippet: Details of the antibodies used in this study and their sources are as follows: FITC-conjugated anti-human PR3 mouse monoclonal antibody (Cat. No. ab65255; Abcam, Cambridge, UK), PE-conjugated anti-human cathepsin D mouse monoclonal antibody (Cat. No. sc-13148 PE; Santa Cruz Biotechnology, Dallas, TX, USA), FITC-conjugated anti-human neutrophil elastase mouse monoclonal antibody (Cat. No. sc-55549 FITC; Santa Cruz Biotechnology, Dallas, TX, USA), PE-conjugated anti-human flavocytochrome b558 mouse monoclonal antibody (Cat. No. D162-5; Medical & Biological Laboratories, Tokyo, Japan), PE/Cyanine7-conjugated anti-human CD14 mouse monoclonal antibody (Cat. No. 367111; BioLegend, San Diego, CA, USA), FITC-conjugated anti-human CD68 mouse monoclonal antibody (Cat. No. F7135; DAKO, Glostrup, Denmark), FITC-conjugated anti-human CD282 (TLR2) mouse monoclonal antibody (Cat. No. 309705; BioLegend, San Diego, CA, USA), PE-conjugated anti-human CD284 (TLR4) mouse monoclonal antibody (Cat. No. 312805; BioLegend, San Diego, CA, USA), anti-citrullinated histone H3 (Cit-H3) (citrulline R2 + R8 + R17) rabbit polyclonal antibody (Cat. No. ab5103; Abcam, Cambridge, UK), anti-human LL-37 mouse monoclonal antibody (Cat. No. sc-166770; Santa Cruz Biotechnology, Dallas, TX, USA), anti-β-actin rabbit monoclonal antibody (Cat. No. 4970; Cell Signaling Technology, Danvers, MA, USA), anti-human CD14 mouse monoclonal antibody (Cat. No. 14-0149-82; Invitrogen, Waltham, MA, USA), anti-PR3 mouse monoclonal antibody (Cat. No. sc-74534; Santa Cruz Biotechnology, Dallas, TX, USA), anti-human presepsin mouse monoclonal antibody (F1106-13–3; Mochida Pharmaceutical, Tokyo, Japan), anti-human presepsin rabbit monoclonal antibody (S68; Mochida Pharmaceutical, Tokyo, Japan), tetramethylrhodamine (TRITC)-conjugated goat anti-mouse IgG (H+L) secondary antibody (Cat. No. SA00007-1; Cosmo Bio, Tokyo, Japan), TRITC-conjugated goat anti-rabbit IgG (H+L) secondary antibody (Cat. No. SA00007-2, Cosmo Bio, Tokyo, Japan), Alexa Flour 405-conjugated goat anti-rabbit IgG (H+L) secondary antibody (Cat. No. ab175652; Invitrogen, Waltham, MA, USA), horseradish peroxidase (HRP)-conjugated goat anti-mouse IgG (H+L) secondary antibody (Cat. No. 7076; Cell Signaling Technology, Danvers, MA, USA), HRP-conjugated gort anti-rabbit IgG (H+L) secondary antibody (Cat. No. 7074; Cell Signaling Technology, Danvers, MA, USA).

    Techniques: Flow Cytometry, Expressing, Enzyme-linked Immunosorbent Assay, Standard Deviation, Western Blot

    Antibodies for Flow Cytometric Identification of Activated Cells in Blood

    Journal: Journal of Inflammation Research

    Article Title: In vitro Validation of a Novel Disposable Remover to Remove Activated Leukocytes Generated During Cardiopulmonary Bypass: A Pilot Study

    doi: 10.2147/JIR.S503575

    Figure Lengend Snippet: Antibodies for Flow Cytometric Identification of Activated Cells in Blood

    Article Snippet: BV421 , CD284 , BV421 Mouse Anti-Human TLR4 (CD284)(TF901) , BD Pharmingen , 564401.

    Techniques: Staining, Blocking Assay

    List of antibodies for FACS analysis used in work.

    Journal: International Journal of Molecular Sciences

    Article Title: Human Liver MSCs Retain Their Basic Cellular Properties in Chronically Inflamed Liver Tissue

    doi: 10.3390/ijms252413374

    Figure Lengend Snippet: List of antibodies for FACS analysis used in work.

    Article Snippet: 20 , APC Anti-Human CD284 (TLR4) , BioLegend , 312815.

    Techniques: