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rabbit monoclonal anti human tlr2 (Cell Signaling Technology Inc)

Name: rabbit monoclonal anti human tlr2
Brand: Cell Signaling Technology Inc
Rating: 95 (93 reviews)

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Cell Signaling Technology Inc rabbit monoclonal anti human tlr2

HRP2 increases pro-inflammatory and Toll-like receptor (TLR) genes in cortical organoids. HRP2-induced inflammation-related genes were profiled Fold changes greater than 1.5 and p values < 0.05 calculated using Student’s t -test was considered to be a significant dysregulation. (A) A heatmap was generated showing up-and down-regulated genes. The effects of HRP2 on cortical organoids at day 50 in culture are shown by site (B), including cerebral cortex and glia, as well as by pathway (C), including TLR signaling. Further analysis revealed the relationship between upregulated genes and activation of <t>TLR2</t> pathway (D). Western blot densitometry of organoid lysates (data represented as means ± SEM) confirms that HRP2 significantly induces TLR2 and TLR1 expression, whereas NRG1 reduces these effects (E, F). a: p < 0.05 compared to basal conditions; b: p < 0.05 compared to HRP2 treatment. One-way ANOVA and t -test were used. Please also see <xref ref-type=

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Rabbit Monoclonal Anti Human Tlr2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 93 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/rabbit monoclonal anti human tlr2/product/Cell Signaling Technology Inc
Average 95 stars, based on 93 article reviews

rabbit monoclonal anti human tlr2 - by Bioz Stars, 2026-02

95/100 stars

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1) Product Images from "Neuregulin-1/ErbB4 signaling modulates Plasmodium falciparum HRP2-induced damage to brain cortical organoids"

Article Title: Neuregulin-1/ErbB4 signaling modulates Plasmodium falciparum HRP2-induced damage to brain cortical organoids

Journal: iScience

doi: 10.1016/j.isci.2022.104407

Figure S4 . " title="... the relationship between upregulated genes and activation of TLR2 pathway (D). Western blot densitometry of organoid lysates ..." property="contentUrl" width="100%" height="100%"/>
Figure Legend Snippet: HRP2 increases pro-inflammatory and Toll-like receptor (TLR) genes in cortical organoids. HRP2-induced inflammation-related genes were profiled Fold changes greater than 1.5 and p values < 0.05 calculated using Student’s t -test was considered to be a significant dysregulation. (A) A heatmap was generated showing up-and down-regulated genes. The effects of HRP2 on cortical organoids at day 50 in culture are shown by site (B), including cerebral cortex and glia, as well as by pathway (C), including TLR signaling. Further analysis revealed the relationship between upregulated genes and activation of TLR2 pathway (D). Western blot densitometry of organoid lysates (data represented as means ± SEM) confirms that HRP2 significantly induces TLR2 and TLR1 expression, whereas NRG1 reduces these effects (E, F). a: p < 0.05 compared to basal conditions; b: p < 0.05 compared to HRP2 treatment. One-way ANOVA and t -test were used. Please also see Figure S4 .

Techniques Used: Generated, Activation Assay, Western Blot, Expressing

HRP2 uses TLR1 and TLR2 to increase CXCL10 expression and cell death in iPSC Cell proliferation, apoptosis, and expression of inflammatory markers were assessed in iPSC treated with HRP2 after TLR1 and TLR2 blockage. (A) Proliferation assay showed that IPSC growth was partially restored, whereas their apoptosis (B) and necrosis (C) were reduced to the levels of untreated controls. TLR1 and TLR2 blocking in HRP2-treated iPSC has an antiapoptotic and anti-inflammatory effect, as it is confirmed by IHC: the expression of cleaved caspase 3 (D, F) and CXCL10 (E, G) is reduced. Data represented as means ± SEM a: p < 0.05 compared to basal conditions; b: p < 0.05 compared to HRP2 treatment. Statistical significance between groups was determined using t -test and analysis of variance.

Figure Legend Snippet: HRP2 uses TLR1 and TLR2 to increase CXCL10 expression and cell death in iPSC Cell proliferation, apoptosis, and expression of inflammatory markers were assessed in iPSC treated with HRP2 after TLR1 and TLR2 blockage. (A) Proliferation assay showed that IPSC growth was partially restored, whereas their apoptosis (B) and necrosis (C) were reduced to the levels of untreated controls. TLR1 and TLR2 blocking in HRP2-treated iPSC has an antiapoptotic and anti-inflammatory effect, as it is confirmed by IHC: the expression of cleaved caspase 3 (D, F) and CXCL10 (E, G) is reduced. Data represented as means ± SEM a: p < 0.05 compared to basal conditions; b: p < 0.05 compared to HRP2 treatment. Statistical significance between groups was determined using t -test and analysis of variance.

Techniques Used: Expressing, Proliferation Assay, Blocking Assay

Figure Legend Snippet:

Techniques Used: Functional Assay, Recombinant, Plasmid Preparation, CCK-8 Assay, Bicinchoninic Acid Protein Assay, Isolation, Gene Expression, Western Blot, Software, Microscopy

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Figure S4 . " width="100%" height="100%">

Journal: iScience

Article Title: Neuregulin-1/ErbB4 signaling modulates Plasmodium falciparum HRP2-induced damage to brain cortical organoids

doi: 10.1016/j.isci.2022.104407

Figure Lengend Snippet: HRP2 increases pro-inflammatory and Toll-like receptor (TLR) genes in cortical organoids. HRP2-induced inflammation-related genes were profiled Fold changes greater than 1.5 and p values < 0.05 calculated using Student’s t -test was considered to be a significant dysregulation. (A) A heatmap was generated showing up-and down-regulated genes. The effects of HRP2 on cortical organoids at day 50 in culture are shown by site (B), including cerebral cortex and glia, as well as by pathway (C), including TLR signaling. Further analysis revealed the relationship between upregulated genes and activation of TLR2 pathway (D). Western blot densitometry of organoid lysates (data represented as means ± SEM) confirms that HRP2 significantly induces TLR2 and TLR1 expression, whereas NRG1 reduces these effects (E, F). a: p < 0.05 compared to basal conditions; b: p < 0.05 compared to HRP2 treatment. One-way ANOVA and t -test were used. Please also see Figure S4 .

Article Snippet: Rabbit monoclonal anti-human TLR2 (clone D769Z) , Cell Signaling , Cat #12276T RRID: AB_2797867.

Techniques: Generated, Activation Assay, Western Blot, Expressing

Journal: iScience

Article Title: Neuregulin-1/ErbB4 signaling modulates Plasmodium falciparum HRP2-induced damage to brain cortical organoids

doi: 10.1016/j.isci.2022.104407

Figure Lengend Snippet: HRP2 uses TLR1 and TLR2 to increase CXCL10 expression and cell death in iPSC Cell proliferation, apoptosis, and expression of inflammatory markers were assessed in iPSC treated with HRP2 after TLR1 and TLR2 blockage. (A) Proliferation assay showed that IPSC growth was partially restored, whereas their apoptosis (B) and necrosis (C) were reduced to the levels of untreated controls. TLR1 and TLR2 blocking in HRP2-treated iPSC has an antiapoptotic and anti-inflammatory effect, as it is confirmed by IHC: the expression of cleaved caspase 3 (D, F) and CXCL10 (E, G) is reduced. Data represented as means ± SEM a: p < 0.05 compared to basal conditions; b: p < 0.05 compared to HRP2 treatment. Statistical significance between groups was determined using t -test and analysis of variance.

Article Snippet: Rabbit monoclonal anti-human TLR2 (clone D769Z) , Cell Signaling , Cat #12276T RRID: AB_2797867.

Techniques: Expressing, Proliferation Assay, Blocking Assay

Journal: iScience

Article Title: Neuregulin-1/ErbB4 signaling modulates Plasmodium falciparum HRP2-induced damage to brain cortical organoids

doi: 10.1016/j.isci.2022.104407

Figure Lengend Snippet:

Article Snippet: Rabbit monoclonal anti-human TLR2 (clone D769Z) , Cell Signaling , Cat #12276T RRID: AB_2797867.

Techniques: Functional Assay, Recombinant, Plasmid Preparation, CCK-8 Assay, Bicinchoninic Acid Protein Assay, Isolation, Gene Expression, Western Blot, Software, Microscopy

Induction of ICAM-1 expression in coronary endothelial cells by PGN and LPS requires TLR2 and TLR4, respectively . A . Coronary endothelial cells isolated from TLR2 KO and wild type (C57BL/6) mice were treated with PGN (10 μg/ml) for 24 h. A representative immunoblot shows that PGN induced a robust increase in ICAM-1 levels in wild type cells, but it had a minimal effect on ICAM-1 levels in TLR2 KO cells. B . A representative immunoblot shows that induction of ICAM-1 expression by LPS (200 ng/ml, 24 h) is markedly reduced in coronary endothelial cells from TLR4-defective (C3H/HeJ) mice.

Journal: Cardiovascular Diabetology

Article Title: Enhanced inflammatory responses to toll-like receptor 2/4 stimulation in type 1 diabetic coronary artery endothelial cells: the effect of insulin

doi: 10.1186/1475-2840-9-90

Figure Lengend Snippet: Induction of ICAM-1 expression in coronary endothelial cells by PGN and LPS requires TLR2 and TLR4, respectively . A . Coronary endothelial cells isolated from TLR2 KO and wild type (C57BL/6) mice were treated with PGN (10 μg/ml) for 24 h. A representative immunoblot shows that PGN induced a robust increase in ICAM-1 levels in wild type cells, but it had a minimal effect on ICAM-1 levels in TLR2 KO cells. B . A representative immunoblot shows that induction of ICAM-1 expression by LPS (200 ng/ml, 24 h) is markedly reduced in coronary endothelial cells from TLR4-defective (C3H/HeJ) mice.

Article Snippet: The following antibodies were used for Western-blot analysis: rabbit anti-human intercellular adhesion molecule (ICAM)-1 (Santa Cruz Biotechnology, Santa Cruz, CA, USA), monoclonal rabbit anti-human TLR2 (Imgenex, San Diego, CA, USA), monoclonal rabbit anti-human TLR4 (Santa Cruz Biotechnology, Santa Cruz, CA, USA), rabbit anti-human phosphor-nuclear factor kappa B (NF-κB) p65 (Cell Signaling, Boston, MA), rabbit anti-human total NF-κB p65 (Cell Signaling, Boston, MA, USA), rabbit anti-human beta-actin (Cell Signaling, Boston, MA, USA), and rabbit anti-mouse ICAM-1 (Santa Cruz Biotechnology, Santa Cruz, CA, USA).

Techniques: Expressing, Isolation, Western Blot

Diabetic CAECs produce and release greater amounts of IL-6 and IL-8 in response to TLR2 and TLR4 stimulation . Non-diabetic and diabetic CAECs were stimulated with PGN (10 μg/ml) and LPS (200 ng/ml) for 1, 2 or 24 h. Levels of IL-6 and IL-8 peptides ( A and B ) in medium were assessed by ELISA after treatment for 24 h, and mRNA levels in cell lysates ( C, D, E and F ) were analyzed with real-time PCR after treatment for 1 or 2 h. After stimulation of either TLR2 or TLR4, diabetic cells expressed higher levels of IL-6 and IL-8 mRNA and released greater amounts of IL-6 and IL-8. Results are expressed as Mean ± SEM; n = 5; * P < 0.05 vs. control; # P < 0.05 vs. non-diabetic cells treated with LPS or PGN.

Journal: Cardiovascular Diabetology

Article Title: Enhanced inflammatory responses to toll-like receptor 2/4 stimulation in type 1 diabetic coronary artery endothelial cells: the effect of insulin

doi: 10.1186/1475-2840-9-90

Figure Lengend Snippet: Diabetic CAECs produce and release greater amounts of IL-6 and IL-8 in response to TLR2 and TLR4 stimulation . Non-diabetic and diabetic CAECs were stimulated with PGN (10 μg/ml) and LPS (200 ng/ml) for 1, 2 or 24 h. Levels of IL-6 and IL-8 peptides ( A and B ) in medium were assessed by ELISA after treatment for 24 h, and mRNA levels in cell lysates ( C, D, E and F ) were analyzed with real-time PCR after treatment for 1 or 2 h. After stimulation of either TLR2 or TLR4, diabetic cells expressed higher levels of IL-6 and IL-8 mRNA and released greater amounts of IL-6 and IL-8. Results are expressed as Mean ± SEM; n = 5; * P < 0.05 vs. control; # P < 0.05 vs. non-diabetic cells treated with LPS or PGN.

Techniques: Enzyme-linked Immunosorbent Assay, Real-time Polymerase Chain Reaction, Control

TLR2 and TLR4 protein levels in diabetic CAECs are not altered . Non-diabetic and diabetic CAECs were untreated or stimulated with PGN (10 μg/ml) or LPS (200 ng/ml) for 24 h. Representative immunoblots shows comparable TLR2 ( A ) and TLR4 ( B ) levels in non-diabetic and diabetic cells with and without stimulation. Results are expressed as Mean ± SEM; n = 5.

Journal: Cardiovascular Diabetology

Article Title: Enhanced inflammatory responses to toll-like receptor 2/4 stimulation in type 1 diabetic coronary artery endothelial cells: the effect of insulin

doi: 10.1186/1475-2840-9-90

Figure Lengend Snippet: TLR2 and TLR4 protein levels in diabetic CAECs are not altered . Non-diabetic and diabetic CAECs were untreated or stimulated with PGN (10 μg/ml) or LPS (200 ng/ml) for 24 h. Representative immunoblots shows comparable TLR2 ( A ) and TLR4 ( B ) levels in non-diabetic and diabetic cells with and without stimulation. Results are expressed as Mean ± SEM; n = 5.

Techniques: Western Blot

NF-κB activation by TLR2 and TLR4 is augmented in diabetic CAECs . Non-diabetic and diabetic CAECs were stimulated with PGN (10 μg/ml) and LPS (200 ng/ml) for 10, 30, 60 or 120 min. A and B . Representative immunoblots show that stimulation of either TLR2 or TLR4 induced greater phosphorylation of NF-κB p65 in diabetic cells at 30 to 120 min. C . NF-κB p65 was label red by immunostaining with a specific antibody, and nuclei were counter-stained blue with bis-benzimide. Representative immunofluorescent images show more intranuclear NF-κB p65 in diabetic cells at 60 min after stimulation of TLR2 or TLR4.

Journal: Cardiovascular Diabetology

Article Title: Enhanced inflammatory responses to toll-like receptor 2/4 stimulation in type 1 diabetic coronary artery endothelial cells: the effect of insulin

doi: 10.1186/1475-2840-9-90

Figure Lengend Snippet: NF-κB activation by TLR2 and TLR4 is augmented in diabetic CAECs . Non-diabetic and diabetic CAECs were stimulated with PGN (10 μg/ml) and LPS (200 ng/ml) for 10, 30, 60 or 120 min. A and B . Representative immunoblots show that stimulation of either TLR2 or TLR4 induced greater phosphorylation of NF-κB p65 in diabetic cells at 30 to 120 min. C . NF-κB p65 was label red by immunostaining with a specific antibody, and nuclei were counter-stained blue with bis-benzimide. Representative immunofluorescent images show more intranuclear NF-κB p65 in diabetic cells at 60 min after stimulation of TLR2 or TLR4.

Techniques: Activation Assay, Western Blot, Phospho-proteomics, Immunostaining, Staining

Insulin has a minor effect on the hyper-inflammatory responses to TLR2 stimulation, but does not affect those to TLR4 stimulation in diabetic CAECs . Insulin (10 or 100 U/l) was added to diabetic CAEC cultures 1 h prior to addition of PGN (10 μg/ml) or LPS (200 ng/ml). Cellular ICAM-1, IL-6 and IL-8 levels were analyzed at 24 h after addition of PGN or LPS. Insulin in a concentration of 10 U/l had no effect on ICAM-1, IL-6 and IL-8 levels following stimulation with either PGN or LPS. Higher concentration of insulin reduced ICAM-1 and IL-6 levels after stimulation with PGN ( A ), but did not affect LPS-induced production of ICAM-1, IL-6 and IL-8 ( B ). Results are expressed as Mean ± SEM; n = 5; *P < 0.05 vs. control.

Journal: Cardiovascular Diabetology

Article Title: Enhanced inflammatory responses to toll-like receptor 2/4 stimulation in type 1 diabetic coronary artery endothelial cells: the effect of insulin

doi: 10.1186/1475-2840-9-90

Figure Lengend Snippet: Insulin has a minor effect on the hyper-inflammatory responses to TLR2 stimulation, but does not affect those to TLR4 stimulation in diabetic CAECs . Insulin (10 or 100 U/l) was added to diabetic CAEC cultures 1 h prior to addition of PGN (10 μg/ml) or LPS (200 ng/ml). Cellular ICAM-1, IL-6 and IL-8 levels were analyzed at 24 h after addition of PGN or LPS. Insulin in a concentration of 10 U/l had no effect on ICAM-1, IL-6 and IL-8 levels following stimulation with either PGN or LPS. Higher concentration of insulin reduced ICAM-1 and IL-6 levels after stimulation with PGN ( A ), but did not affect LPS-induced production of ICAM-1, IL-6 and IL-8 ( B ). Results are expressed as Mean ± SEM; n = 5; *P < 0.05 vs. control.

Techniques: Concentration Assay, Control

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1) Product Images from "Neuregulin-1/ErbB4 signaling modulates Plasmodium falciparum HRP2-induced damage to brain cortical organoids"

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