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mouse tslp elisa kit  (R&D Systems)


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    R&D Systems mouse tslp elisa kit
    PCG suppresses PAR2-induced inflammatory signaling in HaCaT cells. ( A ) Representative immunoblot showing the effect of PCG on ERK1/2 and p65 phosphorylation. HaCaT cells were pretreated with various concentrations of PCG for 20 min before stimulation with 30 µM PAR2-AP. ( B , C ) Quantification of phosphorylated ERK1/2 and p65 levels. Phosphorylated ERK1/2 bands were normalized to total ERK1/2 and phosphorylated p65 (p-p65) was normalized to total p65. ( D ) Effect of PCG on PAR2-AP-induced IL-8 secretion. HaCaT cells were pretreated with PCG for 0 min and then stimulated with 30 µM PAR2-AP for 6 h. IL-8 levels in cell culture supernatants were measured by <t>ELISA.</t> Data are expressed as mean ± SEM ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001.
    Mouse Tslp Elisa Kit, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 50 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/quantikine+mouse+tslp/Mouse+TSLP+Quantikine+ELISA+Kit/pmc12469549-152-8-14
    Average 93 stars, based on 50 article reviews
    mouse tslp elisa kit - by Bioz Stars, 2026-09
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    Images

    1) Product Images from "Blockade of PAR2 Signaling by Punicalagin as a Therapeutic Strategy for Atopic Dermatitis"

    Article Title: Blockade of PAR2 Signaling by Punicalagin as a Therapeutic Strategy for Atopic Dermatitis

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms26188920

    PCG suppresses PAR2-induced inflammatory signaling in HaCaT cells. ( A ) Representative immunoblot showing the effect of PCG on ERK1/2 and p65 phosphorylation. HaCaT cells were pretreated with various concentrations of PCG for 20 min before stimulation with 30 µM PAR2-AP. ( B , C ) Quantification of phosphorylated ERK1/2 and p65 levels. Phosphorylated ERK1/2 bands were normalized to total ERK1/2 and phosphorylated p65 (p-p65) was normalized to total p65. ( D ) Effect of PCG on PAR2-AP-induced IL-8 secretion. HaCaT cells were pretreated with PCG for 0 min and then stimulated with 30 µM PAR2-AP for 6 h. IL-8 levels in cell culture supernatants were measured by ELISA. Data are expressed as mean ± SEM ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001.
    Figure Legend Snippet: PCG suppresses PAR2-induced inflammatory signaling in HaCaT cells. ( A ) Representative immunoblot showing the effect of PCG on ERK1/2 and p65 phosphorylation. HaCaT cells were pretreated with various concentrations of PCG for 20 min before stimulation with 30 µM PAR2-AP. ( B , C ) Quantification of phosphorylated ERK1/2 and p65 levels. Phosphorylated ERK1/2 bands were normalized to total ERK1/2 and phosphorylated p65 (p-p65) was normalized to total p65. ( D ) Effect of PCG on PAR2-AP-induced IL-8 secretion. HaCaT cells were pretreated with PCG for 0 min and then stimulated with 30 µM PAR2-AP for 6 h. IL-8 levels in cell culture supernatants were measured by ELISA. Data are expressed as mean ± SEM ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001.

    Techniques Used: Western Blot, Phospho-proteomics, Cell Culture, Enzyme-linked Immunosorbent Assay

    PCG normalizes epidermal hyperplasia, inflammatory markers, and neuronal hypersensitivity in DNFB-induced atopic dermatitis. ( A ) Representative H&E-stained skin sections showing epidermal thickness on day 28. Scale bar = 100 µm. ( B ) Quantitative analysis of epidermal thickness measured from H&E-stained sections ( n = 5–6 mice per group). ( C ) Serum TSLP levels measured by ELISA. ND, not detected ( n = 5–6 mice per group). ( D ) Calcium imaging of dorsal root ganglion (DRG) neurons in response to PAR2-AP (5 µM) stimulation. Traces show [Ca 2+ ] i changes over time, with KCl (100 mM) used as a positive control for neuronal viability ( n ≥ 20 per group). Data are presented as mean ± SEM. *** p < 0.001 compared to DNFB group.
    Figure Legend Snippet: PCG normalizes epidermal hyperplasia, inflammatory markers, and neuronal hypersensitivity in DNFB-induced atopic dermatitis. ( A ) Representative H&E-stained skin sections showing epidermal thickness on day 28. Scale bar = 100 µm. ( B ) Quantitative analysis of epidermal thickness measured from H&E-stained sections ( n = 5–6 mice per group). ( C ) Serum TSLP levels measured by ELISA. ND, not detected ( n = 5–6 mice per group). ( D ) Calcium imaging of dorsal root ganglion (DRG) neurons in response to PAR2-AP (5 µM) stimulation. Traces show [Ca 2+ ] i changes over time, with KCl (100 mM) used as a positive control for neuronal viability ( n ≥ 20 per group). Data are presented as mean ± SEM. *** p < 0.001 compared to DNFB group.

    Techniques Used: Staining, Enzyme-linked Immunosorbent Assay, Imaging, Positive Control

    Related Articles

    Enzyme-linked Immunosorbent Assay:

    Article Title: Notch-Deficient Skin Induces a Lethal Systemic B-Lymphoproliferative Disorder by Secreting TSLP, a Sentinel for Epidermal Integrity
    Article Snippet: .. Serum TSLP, IL-6, and IL-7 levels were measured according to the manufacturer's instructions in the Quantikine mouse TSLP, IL-6, and IL-7 ELISA kits (R&D Systems). ..

    Article Title: Loss of Grainy Head-Like 1 Is Associated with Disruption of the Epidermal Barrier and Squamous Cell Carcinoma of the Skin
    Article Snippet: .. The blood level of TSLP was measured using enzyme-linked immunosorbent assay (ELISA) kit: Quantikine Mouse TSLP (R&D Systems, Minneapolis, MN, USA) according to the manufacturer’s instructions, on groups of seven Grhl1 −/− and five Grhl1 +/+ animals, at the age of about 4 months. ..



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    PCG suppresses PAR2-induced inflammatory signaling in HaCaT cells. ( A ) Representative immunoblot showing the effect of PCG on ERK1/2 and p65 phosphorylation. HaCaT cells were pretreated with various concentrations of PCG for 20 min before stimulation with 30 µM PAR2-AP. ( B , C ) Quantification of phosphorylated ERK1/2 and p65 levels. Phosphorylated ERK1/2 bands were normalized to total ERK1/2 and phosphorylated p65 (p-p65) was normalized to total p65. ( D ) Effect of PCG on PAR2-AP-induced IL-8 secretion. HaCaT cells were pretreated with PCG for 0 min and then stimulated with 30 µM PAR2-AP for 6 h. IL-8 levels in cell culture supernatants were measured by <t>ELISA.</t> Data are expressed as mean ± SEM ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001.
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    PCG suppresses PAR2-induced inflammatory signaling in HaCaT cells. ( A ) Representative immunoblot showing the effect of PCG on ERK1/2 and p65 phosphorylation. HaCaT cells were pretreated with various concentrations of PCG for 20 min before stimulation with 30 µM PAR2-AP. ( B , C ) Quantification of phosphorylated ERK1/2 and p65 levels. Phosphorylated ERK1/2 bands were normalized to total ERK1/2 and phosphorylated p65 (p-p65) was normalized to total p65. ( D ) Effect of PCG on PAR2-AP-induced IL-8 secretion. HaCaT cells were pretreated with PCG for 0 min and then stimulated with 30 µM PAR2-AP for 6 h. IL-8 levels in cell culture supernatants were measured by <t>ELISA.</t> Data are expressed as mean ± SEM ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001.
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    PCG suppresses PAR2-induced inflammatory signaling in HaCaT cells. ( A ) Representative immunoblot showing the effect of PCG on ERK1/2 and p65 phosphorylation. HaCaT cells were pretreated with various concentrations of PCG for 20 min before stimulation with 30 µM PAR2-AP. ( B , C ) Quantification of phosphorylated ERK1/2 and p65 levels. Phosphorylated ERK1/2 bands were normalized to total ERK1/2 and phosphorylated p65 (p-p65) was normalized to total p65. ( D ) Effect of PCG on PAR2-AP-induced IL-8 secretion. HaCaT cells were pretreated with PCG for 0 min and then stimulated with 30 µM PAR2-AP for 6 h. IL-8 levels in cell culture supernatants were measured by <t>ELISA.</t> Data are expressed as mean ± SEM ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001.
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    PCG suppresses PAR2-induced inflammatory signaling in HaCaT cells. ( A ) Representative immunoblot showing the effect of PCG on ERK1/2 and p65 phosphorylation. HaCaT cells were pretreated with various concentrations of PCG for 20 min before stimulation with 30 µM PAR2-AP. ( B , C ) Quantification of phosphorylated ERK1/2 and p65 levels. Phosphorylated ERK1/2 bands were normalized to total ERK1/2 and phosphorylated p65 (p-p65) was normalized to total p65. ( D ) Effect of PCG on PAR2-AP-induced IL-8 secretion. HaCaT cells were pretreated with PCG for 0 min and then stimulated with 30 µM PAR2-AP for 6 h. IL-8 levels in cell culture supernatants were measured by <t>ELISA.</t> Data are expressed as mean ± SEM ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001.
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    PCG suppresses PAR2-induced inflammatory signaling in HaCaT cells. ( A ) Representative immunoblot showing the effect of PCG on ERK1/2 and p65 phosphorylation. HaCaT cells were pretreated with various concentrations of PCG for 20 min before stimulation with 30 µM PAR2-AP. ( B , C ) Quantification of phosphorylated ERK1/2 and p65 levels. Phosphorylated ERK1/2 bands were normalized to total ERK1/2 and phosphorylated p65 (p-p65) was normalized to total p65. ( D ) Effect of PCG on PAR2-AP-induced IL-8 secretion. HaCaT cells were pretreated with PCG for 0 min and then stimulated with 30 µM PAR2-AP for 6 h. IL-8 levels in cell culture supernatants were measured by <t>ELISA.</t> Data are expressed as mean ± SEM ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001.
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    PCG suppresses PAR2-induced inflammatory signaling in HaCaT cells. ( A ) Representative immunoblot showing the effect of PCG on ERK1/2 and p65 phosphorylation. HaCaT cells were pretreated with various concentrations of PCG for 20 min before stimulation with 30 µM PAR2-AP. ( B , C ) Quantification of phosphorylated ERK1/2 and p65 levels. Phosphorylated ERK1/2 bands were normalized to total ERK1/2 and phosphorylated p65 (p-p65) was normalized to total p65. ( D ) Effect of PCG on PAR2-AP-induced IL-8 secretion. HaCaT cells were pretreated with PCG for 0 min and then stimulated with 30 µM PAR2-AP for 6 h. IL-8 levels in cell culture supernatants were measured by <t>ELISA.</t> Data are expressed as mean ± SEM ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001.
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    PCG suppresses PAR2-induced inflammatory signaling in HaCaT cells. ( A ) Representative immunoblot showing the effect of PCG on ERK1/2 and p65 phosphorylation. HaCaT cells were pretreated with various concentrations of PCG for 20 min before stimulation with 30 µM PAR2-AP. ( B , C ) Quantification of phosphorylated ERK1/2 and p65 levels. Phosphorylated ERK1/2 bands were normalized to total ERK1/2 and phosphorylated p65 (p-p65) was normalized to total p65. ( D ) Effect of PCG on PAR2-AP-induced IL-8 secretion. HaCaT cells were pretreated with PCG for 0 min and then stimulated with 30 µM PAR2-AP for 6 h. IL-8 levels in cell culture supernatants were measured by <t>ELISA.</t> Data are expressed as mean ± SEM ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001.
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    PCG suppresses PAR2-induced inflammatory signaling in HaCaT cells. ( A ) Representative immunoblot showing the effect of PCG on ERK1/2 and p65 phosphorylation. HaCaT cells were pretreated with various concentrations of PCG for 20 min before stimulation with 30 µM PAR2-AP. ( B , C ) Quantification of phosphorylated ERK1/2 and p65 levels. Phosphorylated ERK1/2 bands were normalized to total ERK1/2 and phosphorylated p65 (p-p65) was normalized to total p65. ( D ) Effect of PCG on PAR2-AP-induced IL-8 secretion. HaCaT cells were pretreated with PCG for 0 min and then stimulated with 30 µM PAR2-AP for 6 h. IL-8 levels in cell culture supernatants were measured by ELISA. Data are expressed as mean ± SEM ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001.

    Journal: International Journal of Molecular Sciences

    Article Title: Blockade of PAR2 Signaling by Punicalagin as a Therapeutic Strategy for Atopic Dermatitis

    doi: 10.3390/ijms26188920

    Figure Lengend Snippet: PCG suppresses PAR2-induced inflammatory signaling in HaCaT cells. ( A ) Representative immunoblot showing the effect of PCG on ERK1/2 and p65 phosphorylation. HaCaT cells were pretreated with various concentrations of PCG for 20 min before stimulation with 30 µM PAR2-AP. ( B , C ) Quantification of phosphorylated ERK1/2 and p65 levels. Phosphorylated ERK1/2 bands were normalized to total ERK1/2 and phosphorylated p65 (p-p65) was normalized to total p65. ( D ) Effect of PCG on PAR2-AP-induced IL-8 secretion. HaCaT cells were pretreated with PCG for 0 min and then stimulated with 30 µM PAR2-AP for 6 h. IL-8 levels in cell culture supernatants were measured by ELISA. Data are expressed as mean ± SEM ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001.

    Article Snippet: The levels of TSLP were measured using a mouse TSLP ELISA kit (catalog #MTLP00; R&D Systems, Minneapolis, MN, USA) according to the manufacturer’s protocol.

    Techniques: Western Blot, Phospho-proteomics, Cell Culture, Enzyme-linked Immunosorbent Assay

    PCG normalizes epidermal hyperplasia, inflammatory markers, and neuronal hypersensitivity in DNFB-induced atopic dermatitis. ( A ) Representative H&E-stained skin sections showing epidermal thickness on day 28. Scale bar = 100 µm. ( B ) Quantitative analysis of epidermal thickness measured from H&E-stained sections ( n = 5–6 mice per group). ( C ) Serum TSLP levels measured by ELISA. ND, not detected ( n = 5–6 mice per group). ( D ) Calcium imaging of dorsal root ganglion (DRG) neurons in response to PAR2-AP (5 µM) stimulation. Traces show [Ca 2+ ] i changes over time, with KCl (100 mM) used as a positive control for neuronal viability ( n ≥ 20 per group). Data are presented as mean ± SEM. *** p < 0.001 compared to DNFB group.

    Journal: International Journal of Molecular Sciences

    Article Title: Blockade of PAR2 Signaling by Punicalagin as a Therapeutic Strategy for Atopic Dermatitis

    doi: 10.3390/ijms26188920

    Figure Lengend Snippet: PCG normalizes epidermal hyperplasia, inflammatory markers, and neuronal hypersensitivity in DNFB-induced atopic dermatitis. ( A ) Representative H&E-stained skin sections showing epidermal thickness on day 28. Scale bar = 100 µm. ( B ) Quantitative analysis of epidermal thickness measured from H&E-stained sections ( n = 5–6 mice per group). ( C ) Serum TSLP levels measured by ELISA. ND, not detected ( n = 5–6 mice per group). ( D ) Calcium imaging of dorsal root ganglion (DRG) neurons in response to PAR2-AP (5 µM) stimulation. Traces show [Ca 2+ ] i changes over time, with KCl (100 mM) used as a positive control for neuronal viability ( n ≥ 20 per group). Data are presented as mean ± SEM. *** p < 0.001 compared to DNFB group.

    Article Snippet: The levels of TSLP were measured using a mouse TSLP ELISA kit (catalog #MTLP00; R&D Systems, Minneapolis, MN, USA) according to the manufacturer’s protocol.

    Techniques: Staining, Enzyme-linked Immunosorbent Assay, Imaging, Positive Control