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Bioss rabbit polyclonal antibody against tlr2

(A-B) High pulsatility flow (HPF), due to the use of a “stiff” tube upstream to cell culture, upregulated proinflammatory molecule mRNA (ICAM-1, VCAM-1, MCP-1 and E-selectin) and protein (MCP-1) in healthy PAECs, compared to low pulsatility flow (LPF) or to static conditions. (C-D) The mRNA and protein expression of <t>TLR2</t> but not TLR4 in PAECs was highly upregulated by HPF. *: p<0.05 versus Static, †: p<0.05 versus LPF.

Rabbit Polyclonal Antibody Against Tlr2, supplied by Bioss, used in various techniques. Bioz Stars score: 94/100, based on 37 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 94 stars, based on 37 article reviews

rabbit polyclonal antibody against tlr2 - by Bioz Stars, 2026-06

94/100 stars

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1) Product Images from "Stiffening-Induced High Pulsatility Flow Activates Endothelial Inflammation via a TLR2/NF-κB Pathway"

Article Title: Stiffening-Induced High Pulsatility Flow Activates Endothelial Inflammation via a TLR2/NF-κB Pathway

Journal: PLoS ONE

doi: 10.1371/journal.pone.0102195

Figure Legend Snippet: (A-B) High pulsatility flow (HPF), due to the use of a “stiff” tube upstream to cell culture, upregulated proinflammatory molecule mRNA (ICAM-1, VCAM-1, MCP-1 and E-selectin) and protein (MCP-1) in healthy PAECs, compared to low pulsatility flow (LPF) or to static conditions. (C-D) The mRNA and protein expression of TLR2 but not TLR4 in PAECs was highly upregulated by HPF. *: p<0.05 versus Static, †: p<0.05 versus LPF.

Techniques Used: Cell Culture, Expressing

(A, C) At the mRNA level, TLR2/4 inhibitor OxPAPC or TLR2 siRNA but not TLR4 inhibitor CLI-095, decreased PAEC expression of ICAM-1, VCAM-1, MCP-1 and E-selectin mRNAs under HPF; TLR4 siRNA decreased ICAM-1 and E-selectin but not VCAM-1 and MCP-1 mRNAs. “*”: p<0.05 versus LPF, “†”: p<0.05 versus HPF. (B, D) At the protein level, the MCP-1 expression in PAECs exposed to HPF was inhibited by OxPAPC or TLR2 siRNA treatment but not CLI-095 or TLR4 siRNA. The black line in the blot images (D, right) shows separated lanes obtained on the same gel.

Figure Legend Snippet: (A, C) At the mRNA level, TLR2/4 inhibitor OxPAPC or TLR2 siRNA but not TLR4 inhibitor CLI-095, decreased PAEC expression of ICAM-1, VCAM-1, MCP-1 and E-selectin mRNAs under HPF; TLR4 siRNA decreased ICAM-1 and E-selectin but not VCAM-1 and MCP-1 mRNAs. “*”: p<0.05 versus LPF, “†”: p<0.05 versus HPF. (B, D) At the protein level, the MCP-1 expression in PAECs exposed to HPF was inhibited by OxPAPC or TLR2 siRNA treatment but not CLI-095 or TLR4 siRNA. The black line in the blot images (D, right) shows separated lanes obtained on the same gel.

Techniques Used: Expressing

Pulse flow modulates TLR2-induced NF-κB activation in BPAECs. (A) Representative fluorescent images and quantitative measures of NF-kBp65 staining (red) in PAECs show HPF stimulation of PAECs led to increased intranuclear translocation or activation of NF-κB, which was reduced by TLR2/4 inhibitor OxPAPC and TLR2 siRNA. Blue stains show the nuclei. The scale bar shows 50 µm. (B) HPF stimulation of PAECs increased the mRNA levels of IKKα and IKKβ, both of which were attenuated in siRNA-transfected cells with knockdown of TLR2. (C) NF-κB inhibitor (BAY 11–7082) decreased the MCP-1 expression by PAECs exposed to HPF. *: p<0.05 versus LPF, †: p<0.05 versus HPF.

Figure Legend Snippet: Pulse flow modulates TLR2-induced NF-κB activation in BPAECs. (A) Representative fluorescent images and quantitative measures of NF-kBp65 staining (red) in PAECs show HPF stimulation of PAECs led to increased intranuclear translocation or activation of NF-κB, which was reduced by TLR2/4 inhibitor OxPAPC and TLR2 siRNA. Blue stains show the nuclei. The scale bar shows 50 µm. (B) HPF stimulation of PAECs increased the mRNA levels of IKKα and IKKβ, both of which were attenuated in siRNA-transfected cells with knockdown of TLR2. (C) NF-κB inhibitor (BAY 11–7082) decreased the MCP-1 expression by PAECs exposed to HPF. *: p<0.05 versus LPF, †: p<0.05 versus HPF.

Techniques Used: Activation Assay, Staining, Translocation Assay, Transfection, Expressing

(A) PAECs from calves with hypoxia-induced pulmonary hypertension (PH) show elevated expression of TLR2 and TLR4, compared to control (CO). *:p<0.05. (B) Both immunostaining and western blotting results show elevated MCP-1 expression by PH-ECs compared to CO-ECs from calves. “PA” indicates the lumen of a pulmonary artery. *:p<0.05. (C) Enhanced TLR2 expression in the pulmonary arterial endothelium of human with pulmonary arterial hypertension (PAH). Cryosections of human intra-lobar pulmonary arteries were immunostained with TLR2 (red fluorescence) and counterstained with DAPI (cell nuclei, blue). Elastic lamellae showed green auto-fluorescence.

Figure Legend Snippet: (A) PAECs from calves with hypoxia-induced pulmonary hypertension (PH) show elevated expression of TLR2 and TLR4, compared to control (CO). *:p<0.05. (B) Both immunostaining and western blotting results show elevated MCP-1 expression by PH-ECs compared to CO-ECs from calves. “PA” indicates the lumen of a pulmonary artery. *:p<0.05. (C) Enhanced TLR2 expression in the pulmonary arterial endothelium of human with pulmonary arterial hypertension (PAH). Cryosections of human intra-lobar pulmonary arteries were immunostained with TLR2 (red fluorescence) and counterstained with DAPI (cell nuclei, blue). Elastic lamellae showed green auto-fluorescence.

Techniques Used: Expressing, Immunostaining, Western Blot, Fluorescence

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Journal: PLoS ONE

Article Title: Stiffening-Induced High Pulsatility Flow Activates Endothelial Inflammation via a TLR2/NF-κB Pathway

doi: 10.1371/journal.pone.0102195

Figure Lengend Snippet: (A-B) High pulsatility flow (HPF), due to the use of a “stiff” tube upstream to cell culture, upregulated proinflammatory molecule mRNA (ICAM-1, VCAM-1, MCP-1 and E-selectin) and protein (MCP-1) in healthy PAECs, compared to low pulsatility flow (LPF) or to static conditions. (C-D) The mRNA and protein expression of TLR2 but not TLR4 in PAECs was highly upregulated by HPF. *: p<0.05 versus Static, †: p<0.05 versus LPF.

Article Snippet: Antibodies used here include: rabbit polyclonal antibody against bovine MCP-1 (1∶500 dilution; Kingfisher Biotech, St. Paul, MN), rabbit polyclonal antibody against TLR2 (1∶100 dilution; Bioss Inc, Woburn MA), mouse monoclonal antibody against TLR4 (1∶100 dilution; Acris Antibodies Inc, San Diego, CA) and mouse monoclonal antibody against GAPDH (1∶20,000 dilution; Sigma Inc, Saint Louis, MO).

Techniques: Cell Culture, Expressing

Journal: PLoS ONE

Article Title: Stiffening-Induced High Pulsatility Flow Activates Endothelial Inflammation via a TLR2/NF-κB Pathway

doi: 10.1371/journal.pone.0102195

Figure Lengend Snippet: (A, C) At the mRNA level, TLR2/4 inhibitor OxPAPC or TLR2 siRNA but not TLR4 inhibitor CLI-095, decreased PAEC expression of ICAM-1, VCAM-1, MCP-1 and E-selectin mRNAs under HPF; TLR4 siRNA decreased ICAM-1 and E-selectin but not VCAM-1 and MCP-1 mRNAs. “*”: p<0.05 versus LPF, “†”: p<0.05 versus HPF. (B, D) At the protein level, the MCP-1 expression in PAECs exposed to HPF was inhibited by OxPAPC or TLR2 siRNA treatment but not CLI-095 or TLR4 siRNA. The black line in the blot images (D, right) shows separated lanes obtained on the same gel.

Techniques: Expressing

Journal: PLoS ONE

Article Title: Stiffening-Induced High Pulsatility Flow Activates Endothelial Inflammation via a TLR2/NF-κB Pathway

doi: 10.1371/journal.pone.0102195

Figure Lengend Snippet: Pulse flow modulates TLR2-induced NF-κB activation in BPAECs. (A) Representative fluorescent images and quantitative measures of NF-kBp65 staining (red) in PAECs show HPF stimulation of PAECs led to increased intranuclear translocation or activation of NF-κB, which was reduced by TLR2/4 inhibitor OxPAPC and TLR2 siRNA. Blue stains show the nuclei. The scale bar shows 50 µm. (B) HPF stimulation of PAECs increased the mRNA levels of IKKα and IKKβ, both of which were attenuated in siRNA-transfected cells with knockdown of TLR2. (C) NF-κB inhibitor (BAY 11–7082) decreased the MCP-1 expression by PAECs exposed to HPF. *: p<0.05 versus LPF, †: p<0.05 versus HPF.

Techniques: Activation Assay, Staining, Translocation Assay, Transfection, Expressing

Journal: PLoS ONE

Article Title: Stiffening-Induced High Pulsatility Flow Activates Endothelial Inflammation via a TLR2/NF-κB Pathway

doi: 10.1371/journal.pone.0102195

Figure Lengend Snippet: (A) PAECs from calves with hypoxia-induced pulmonary hypertension (PH) show elevated expression of TLR2 and TLR4, compared to control (CO). *:p<0.05. (B) Both immunostaining and western blotting results show elevated MCP-1 expression by PH-ECs compared to CO-ECs from calves. “PA” indicates the lumen of a pulmonary artery. *:p<0.05. (C) Enhanced TLR2 expression in the pulmonary arterial endothelium of human with pulmonary arterial hypertension (PAH). Cryosections of human intra-lobar pulmonary arteries were immunostained with TLR2 (red fluorescence) and counterstained with DAPI (cell nuclei, blue). Elastic lamellae showed green auto-fluorescence.

Techniques: Expressing, Immunostaining, Western Blot, Fluorescence

MPs induce inflammation by recognizing TLR2/4 in BMDMs. (A) Representative Western blot images of BMDMs treated with MPs or LPS (positive control) for 24 h. TLR2, TLR4, TIRAP, MyD88, TRAF6, P-JNK, and P-c-Jun protein expression levels, analyzed by Western blotting. β-actin expression was used as a loading CTL. (B) Relative mRNA expression levels of Il-1β , Il-6 , and Tnf-α , measured in the presence of MP. Gapdh was used for normalization. (C) Representative flow cytometry plots presenting BMDM M1 and M2 polarization upon MP treatment. The M1 and M2 macrophage populations were quantified as CD86 + CD206 – and CD86 – CD206 + , respectively. (D) Representative immunofluorescence images of BMDMs treated with or without MPs for 24 h, stained with MPO (green), CitH3 (red), and DAPI (blue). Scale bars, 10 μm. Fluorescence intensity-based MPO and CitH3 quantification in BMDMs. a.u., arbitrary unit. The data represent at least three independent experiments and are expressed as the mean ± SEM, using one-way ANOVA. **** p < 0.0001, *** p < 0.001, ** p < 0.01, * p < 0.05.

Journal: ACS Nano

Article Title: Microplastic-Induced Macrophage Dysfunction Drives Lung Tumor Progression through Glutathione Imbalance

doi: 10.1021/acsnano.5c15425

Figure Lengend Snippet: MPs induce inflammation by recognizing TLR2/4 in BMDMs. (A) Representative Western blot images of BMDMs treated with MPs or LPS (positive control) for 24 h. TLR2, TLR4, TIRAP, MyD88, TRAF6, P-JNK, and P-c-Jun protein expression levels, analyzed by Western blotting. β-actin expression was used as a loading CTL. (B) Relative mRNA expression levels of Il-1β , Il-6 , and Tnf-α , measured in the presence of MP. Gapdh was used for normalization. (C) Representative flow cytometry plots presenting BMDM M1 and M2 polarization upon MP treatment. The M1 and M2 macrophage populations were quantified as CD86 + CD206 – and CD86 – CD206 + , respectively. (D) Representative immunofluorescence images of BMDMs treated with or without MPs for 24 h, stained with MPO (green), CitH3 (red), and DAPI (blue). Scale bars, 10 μm. Fluorescence intensity-based MPO and CitH3 quantification in BMDMs. a.u., arbitrary unit. The data represent at least three independent experiments and are expressed as the mean ± SEM, using one-way ANOVA. **** p < 0.0001, *** p < 0.001, ** p < 0.01, * p < 0.05.

Article Snippet: Each membrane was incubated overnight at 4 °C with primary antibodies against TLR2 (Cell Signaling Technology, 13744S), TLR4 (Proteintech, 66350–1-Ig), TIRAP (Cell Signaling Technology, 13077), MyD88 (Cell Signaling Technology, 4283), TRAF6 (Cell Signaling Technology, 67591), P-JNK (Cell Signaling Technology, 9251), P-c-Jun (Cell Signaling Technology, 3270), NRF2 (Cell Signaling Technology, 12721), GCLM (Abcam, ab126704), SLC7A11 (Novus Biologicals, NB300–318), NQO1 (Santa Cruz Biotechnology, sc-32793), GCLC (Cell Signaling Technology, 52183), GPX1 (R&D systems, AF3798), GPX3 (R&D systems, AF4199), GPX4 (R&D systems, MAB5457), FTL (Santa Cruz Biotechnology, sc-390558;), FTH1 (Santa Cruz Biotechnology, sc-376594), and β-actin (Cell Signaling Technology, 8457).

Techniques: Western Blot, Positive Control, Expressing, Flow Cytometry, Immunofluorescence, Staining, Fluorescence

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