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anti mapk phosphatase 1 mkp 1 monoclonal antibody  (Santa Cruz Biotechnology)


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    Structured Review

    Santa Cruz Biotechnology anti mapk phosphatase 1 mkp 1 monoclonal antibody
    Molecular mechanisms resulting in steroid unresponsiveness, induced by co-stimulation of TWEAK and TGF-β1. The mRNA levels of <t>MKP-1</t> ( A ), GILZ ( C ), GRβ ( E ), and HDAC2 ( F ) mRNA after 48 h treatment, analyzed by qRT–PCR. MAP kinase phosphatase 1 (MKP-1) and glucocorticoid-induced leucine zipper (GILZ) levels analyzed by immunoblotting ( B , D , upper panel). Densitometric analysis of protein bands ( B , D , lower). Data represent mean ± SD of two independent experiments. * p < 0.05, compared to untreated cultures as controls; † p < 0.05 compared with cultures in the absence of DEX.
    Anti Mapk Phosphatase 1 Mkp 1 Monoclonal Antibody, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 518 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mapk+phosphatase-1/MKP-1+Antibody/pmc11546882-105-0-16
    Average 94 stars, based on 518 article reviews
    anti mapk phosphatase 1 mkp 1 monoclonal antibody - by Bioz Stars, 2026-09
    94/100 stars

    Images

    1) Product Images from "Co-Stimulation with TWEAK and TGF-β1 Induces Steroid-Insensitive TSLP and CCL5 Production in BEAS-2B Human Bronchial Epithelial Cells"

    Article Title: Co-Stimulation with TWEAK and TGF-β1 Induces Steroid-Insensitive TSLP and CCL5 Production in BEAS-2B Human Bronchial Epithelial Cells

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms252111625

    Molecular mechanisms resulting in steroid unresponsiveness, induced by co-stimulation of TWEAK and TGF-β1. The mRNA levels of MKP-1 ( A ), GILZ ( C ), GRβ ( E ), and HDAC2 ( F ) mRNA after 48 h treatment, analyzed by qRT–PCR. MAP kinase phosphatase 1 (MKP-1) and glucocorticoid-induced leucine zipper (GILZ) levels analyzed by immunoblotting ( B , D , upper panel). Densitometric analysis of protein bands ( B , D , lower). Data represent mean ± SD of two independent experiments. * p < 0.05, compared to untreated cultures as controls; † p < 0.05 compared with cultures in the absence of DEX.
    Figure Legend Snippet: Molecular mechanisms resulting in steroid unresponsiveness, induced by co-stimulation of TWEAK and TGF-β1. The mRNA levels of MKP-1 ( A ), GILZ ( C ), GRβ ( E ), and HDAC2 ( F ) mRNA after 48 h treatment, analyzed by qRT–PCR. MAP kinase phosphatase 1 (MKP-1) and glucocorticoid-induced leucine zipper (GILZ) levels analyzed by immunoblotting ( B , D , upper panel). Densitometric analysis of protein bands ( B , D , lower). Data represent mean ± SD of two independent experiments. * p < 0.05, compared to untreated cultures as controls; † p < 0.05 compared with cultures in the absence of DEX.

    Techniques Used: Quantitative RT-PCR, Western Blot

    Co-stimulation of TWEAK and TGF-β1 induces steroid-unresponsive production of cytokines through the mitogen-activated protein kinase and nuclear factor kappa beta signaling pathways. Confluent monolayers of BEAS-2B cells were cultured for 48 h in the absence (DMSO as vehicle) or presence of AZD6244 (5 μM), SB202190 (5 μM), SP600125 (5 μM), or BAY11-7082 (2.5 μM) and treated with TGF-β1 (10 ng/mL), TWEAK (100 ng/mL), or TGF-β1 in combination with TWEAK. The mRNA levels of TSLP ( A ), CCL5 ( B ), MKP-1 ( C ), and GILZ ( D ) were analyzed by qRT–PCR. Data represent mean ± SD of two independent experiments. * p < 0.05, compared with the vehicle; † p < 0.05 compared with cultures in the absence of DEX.
    Figure Legend Snippet: Co-stimulation of TWEAK and TGF-β1 induces steroid-unresponsive production of cytokines through the mitogen-activated protein kinase and nuclear factor kappa beta signaling pathways. Confluent monolayers of BEAS-2B cells were cultured for 48 h in the absence (DMSO as vehicle) or presence of AZD6244 (5 μM), SB202190 (5 μM), SP600125 (5 μM), or BAY11-7082 (2.5 μM) and treated with TGF-β1 (10 ng/mL), TWEAK (100 ng/mL), or TGF-β1 in combination with TWEAK. The mRNA levels of TSLP ( A ), CCL5 ( B ), MKP-1 ( C ), and GILZ ( D ) were analyzed by qRT–PCR. Data represent mean ± SD of two independent experiments. * p < 0.05, compared with the vehicle; † p < 0.05 compared with cultures in the absence of DEX.

    Techniques Used: Protein-Protein interactions, Cell Culture, Quantitative RT-PCR

    MKP-1 is involved in steroid unresponsiveness induced by co-stimulation with TWEAK and TGF-β1 in BEAS-2B cells. The mRNA levels of MKP-1 ( A ), TSLP ( C ), and CCL5 ( E ), analyzed by qRT–PCR. Data represent mean ± SD of two independent experiments. MKP-1 and thymic stromal lymphopoietin (TSLP) expression after 48 h of treatment, assessed by immunoblotting ( B , D , upper panel). Densitometric analysis of protein bands ( B , D , lower). The level of CCL5 in cell culture supernatants after 48 h of treatment, analyzed using ELISA ( F ). Data represent mean ± SD of two independent experiments. * p < 0.05, compared to untreated cultures as controls; † p < 0.05 compared with cultures in the absence of DEX; ‡ p < 0.05 compared with control siRNA.
    Figure Legend Snippet: MKP-1 is involved in steroid unresponsiveness induced by co-stimulation with TWEAK and TGF-β1 in BEAS-2B cells. The mRNA levels of MKP-1 ( A ), TSLP ( C ), and CCL5 ( E ), analyzed by qRT–PCR. Data represent mean ± SD of two independent experiments. MKP-1 and thymic stromal lymphopoietin (TSLP) expression after 48 h of treatment, assessed by immunoblotting ( B , D , upper panel). Densitometric analysis of protein bands ( B , D , lower). The level of CCL5 in cell culture supernatants after 48 h of treatment, analyzed using ELISA ( F ). Data represent mean ± SD of two independent experiments. * p < 0.05, compared to untreated cultures as controls; † p < 0.05 compared with cultures in the absence of DEX; ‡ p < 0.05 compared with control siRNA.

    Techniques Used: Quantitative RT-PCR, Expressing, Western Blot, Cell Culture, Enzyme-linked Immunosorbent Assay, Control

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    Image Search Results


    Molecular mechanisms resulting in steroid unresponsiveness, induced by co-stimulation of TWEAK and TGF-β1. The mRNA levels of MKP-1 ( A ), GILZ ( C ), GRβ ( E ), and HDAC2 ( F ) mRNA after 48 h treatment, analyzed by qRT–PCR. MAP kinase phosphatase 1 (MKP-1) and glucocorticoid-induced leucine zipper (GILZ) levels analyzed by immunoblotting ( B , D , upper panel). Densitometric analysis of protein bands ( B , D , lower). Data represent mean ± SD of two independent experiments. * p < 0.05, compared to untreated cultures as controls; † p < 0.05 compared with cultures in the absence of DEX.

    Journal: International Journal of Molecular Sciences

    Article Title: Co-Stimulation with TWEAK and TGF-β1 Induces Steroid-Insensitive TSLP and CCL5 Production in BEAS-2B Human Bronchial Epithelial Cells

    doi: 10.3390/ijms252111625

    Figure Lengend Snippet: Molecular mechanisms resulting in steroid unresponsiveness, induced by co-stimulation of TWEAK and TGF-β1. The mRNA levels of MKP-1 ( A ), GILZ ( C ), GRβ ( E ), and HDAC2 ( F ) mRNA after 48 h treatment, analyzed by qRT–PCR. MAP kinase phosphatase 1 (MKP-1) and glucocorticoid-induced leucine zipper (GILZ) levels analyzed by immunoblotting ( B , D , upper panel). Densitometric analysis of protein bands ( B , D , lower). Data represent mean ± SD of two independent experiments. * p < 0.05, compared to untreated cultures as controls; † p < 0.05 compared with cultures in the absence of DEX.

    Article Snippet: Anti-MAPK phosphatase-1 (MKP-1) monoclonal antibody (sc-271684) and anti-glucocorticoid-induced leucine zipper (GILZ) mAb (G-5) were purchased from Santa Cruz Biotechnology (Santa Cruz, CA, USA).

    Techniques: Quantitative RT-PCR, Western Blot

    Co-stimulation of TWEAK and TGF-β1 induces steroid-unresponsive production of cytokines through the mitogen-activated protein kinase and nuclear factor kappa beta signaling pathways. Confluent monolayers of BEAS-2B cells were cultured for 48 h in the absence (DMSO as vehicle) or presence of AZD6244 (5 μM), SB202190 (5 μM), SP600125 (5 μM), or BAY11-7082 (2.5 μM) and treated with TGF-β1 (10 ng/mL), TWEAK (100 ng/mL), or TGF-β1 in combination with TWEAK. The mRNA levels of TSLP ( A ), CCL5 ( B ), MKP-1 ( C ), and GILZ ( D ) were analyzed by qRT–PCR. Data represent mean ± SD of two independent experiments. * p < 0.05, compared with the vehicle; † p < 0.05 compared with cultures in the absence of DEX.

    Journal: International Journal of Molecular Sciences

    Article Title: Co-Stimulation with TWEAK and TGF-β1 Induces Steroid-Insensitive TSLP and CCL5 Production in BEAS-2B Human Bronchial Epithelial Cells

    doi: 10.3390/ijms252111625

    Figure Lengend Snippet: Co-stimulation of TWEAK and TGF-β1 induces steroid-unresponsive production of cytokines through the mitogen-activated protein kinase and nuclear factor kappa beta signaling pathways. Confluent monolayers of BEAS-2B cells were cultured for 48 h in the absence (DMSO as vehicle) or presence of AZD6244 (5 μM), SB202190 (5 μM), SP600125 (5 μM), or BAY11-7082 (2.5 μM) and treated with TGF-β1 (10 ng/mL), TWEAK (100 ng/mL), or TGF-β1 in combination with TWEAK. The mRNA levels of TSLP ( A ), CCL5 ( B ), MKP-1 ( C ), and GILZ ( D ) were analyzed by qRT–PCR. Data represent mean ± SD of two independent experiments. * p < 0.05, compared with the vehicle; † p < 0.05 compared with cultures in the absence of DEX.

    Article Snippet: Anti-MAPK phosphatase-1 (MKP-1) monoclonal antibody (sc-271684) and anti-glucocorticoid-induced leucine zipper (GILZ) mAb (G-5) were purchased from Santa Cruz Biotechnology (Santa Cruz, CA, USA).

    Techniques: Protein-Protein interactions, Cell Culture, Quantitative RT-PCR

    MKP-1 is involved in steroid unresponsiveness induced by co-stimulation with TWEAK and TGF-β1 in BEAS-2B cells. The mRNA levels of MKP-1 ( A ), TSLP ( C ), and CCL5 ( E ), analyzed by qRT–PCR. Data represent mean ± SD of two independent experiments. MKP-1 and thymic stromal lymphopoietin (TSLP) expression after 48 h of treatment, assessed by immunoblotting ( B , D , upper panel). Densitometric analysis of protein bands ( B , D , lower). The level of CCL5 in cell culture supernatants after 48 h of treatment, analyzed using ELISA ( F ). Data represent mean ± SD of two independent experiments. * p < 0.05, compared to untreated cultures as controls; † p < 0.05 compared with cultures in the absence of DEX; ‡ p < 0.05 compared with control siRNA.

    Journal: International Journal of Molecular Sciences

    Article Title: Co-Stimulation with TWEAK and TGF-β1 Induces Steroid-Insensitive TSLP and CCL5 Production in BEAS-2B Human Bronchial Epithelial Cells

    doi: 10.3390/ijms252111625

    Figure Lengend Snippet: MKP-1 is involved in steroid unresponsiveness induced by co-stimulation with TWEAK and TGF-β1 in BEAS-2B cells. The mRNA levels of MKP-1 ( A ), TSLP ( C ), and CCL5 ( E ), analyzed by qRT–PCR. Data represent mean ± SD of two independent experiments. MKP-1 and thymic stromal lymphopoietin (TSLP) expression after 48 h of treatment, assessed by immunoblotting ( B , D , upper panel). Densitometric analysis of protein bands ( B , D , lower). The level of CCL5 in cell culture supernatants after 48 h of treatment, analyzed using ELISA ( F ). Data represent mean ± SD of two independent experiments. * p < 0.05, compared to untreated cultures as controls; † p < 0.05 compared with cultures in the absence of DEX; ‡ p < 0.05 compared with control siRNA.

    Article Snippet: Anti-MAPK phosphatase-1 (MKP-1) monoclonal antibody (sc-271684) and anti-glucocorticoid-induced leucine zipper (GILZ) mAb (G-5) were purchased from Santa Cruz Biotechnology (Santa Cruz, CA, USA).

    Techniques: Quantitative RT-PCR, Expressing, Western Blot, Cell Culture, Enzyme-linked Immunosorbent Assay, Control