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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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    Article Title: Depletion of cyclic‐GMP levels and inhibition of cGMP‐dependent protein kinase activate p21 Cip1 /p27 Kip1 pathways and lead to renal fibrosis and dysfunction
    Article Snippet: Primary antibodies of cGMP‐dependent protein kinase 1 (cGK I), cGK II, proliferating cell nuclear antigen (PCNA), MAPK phosphatase‐1 (MKP‐1), p‐Erk1/2, p‐p38, p21 Cip1 , and p27 Kip1 were obtained from Santa Cruz Biotechnology (San Diego, CA, USA).

    Article Title: Inhibition of lipopolysaccharide-induced inducible nitric oxide synthase expression by endoplasmic reticulum stress.
    Article Snippet: a Department of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan b Department of Internal Medicine, Tao-Yuan General Hospital Department of Health the Executive Yuan, Taoyuan, Taiwan c Department of Biomedical Engineering, Chung Yuan Christian University, Taoyuan, Taiwan d Department of Family Medicine of National Taiwan University Hospital, Taipei, Taiwan e Graduate Institute of Medical Sciences, Taipei Medical University, Taipei, Taiwan

    Article Title: Depletion of cyclic‐GMP levels and inhibition of cGMP‐dependent protein kinase activate p21 Cip1 /p27 Kip1 pathways and lead to renal fibrosis and dysfunction
    Article Snippet: Primary antibodies of cGMP-dependent protein kinase 1 (cGK I), cGK II, proliferating cell nuclear antigen (PCNA), MAPK phosphatase-1 (MKP-1), p-Erk1/2, p-p38, p21Cip1, and p27Kip1 were obtained from Santa Cruz Biotechnology (San Diego, CA, USA).

    Article Title: Identification of DUOX1-dependent redox signaling through protein S -glutathionylation in airway epithelial cells
    Article Snippet: Eluted protein and corresponding whole cell lysates (as input controls) were mixed with reducing sample buffer for analysis by SDS-PAGE, transferred to PVDF, and blotted with using antibodies against β-actin (Cell Signaling), peroxiredoxin 1 (Prx1; Abcam), c-Src (L4A1; Cell Signaling), and MAPK phosphatase 1 (MKP-1; Santa Cruz).

    Article Title: Antioxidant and anti-inflammatory effects in RAW264.7 macrophages of malvidin, a major red wine polyphenol.
    Article Snippet: Antibody against N-terminal domain of actin was obtained from Sigma-Aldrich Co. (Budapest, Hungary), and MAPK phosphatase-1 (MKP-1), Histon H-1 antibodies were from Santa Cruz Biotechnology (Santa Cruz, CA, USA).

    Western Blot:

    Article Title: Methylprednisolone blocks autoantibody-induced tissue damage in experimental models of bullous pemphigoid and epidermolysis bullosa acquisita through inhibition of neutrophil activation.
    Article Snippet: .. An equivalent of 0.75 million cells was used for western blot analysis with antibodies against phospho Akt (Thr308), phospho ERK1/2, phospho p38 MAPK, or b-actin (all from Cell Signaling Technology) or MAPK phosphatase-1 (Santa Cruz Biotechnology, Santa Cruz, CA). ..

    Article Title: c-Jun-mediated anticancer mechanisms of tylophorine.
    Article Snippet: Chemicals and reagents were purchased from the following sources: high-performance liquid chromatography-grade DMSO, nocodazole, thymidine and propidium iodide were from Sigma–Aldrich (St Louis, MO); anisomycin, phorbol 12-myristate 13-acetate, SP600125, PD98095, SB203580 and LY294002 were from BioSource, Invitrogen (Carlsbad, CA); GF1092004X, cycloheximide, rottlerin, IMD0354, BX795, rapamycin, triciribine and okadaic acid were from Merck Millipore Calbiochem (Billerica, MA); FuGENE 6 transfection reagent was from Roche Diagnostics GmbH, (Mannheim, Germany) and pNF-κB-Luc and pAP1-Luc were from Stratagene (La Jolla, CA). .. Western blotting was performed as described previously (6,20) with antibodies targeted against β-actin (Millipore Merck Chemicon, Pittsburgh, PA); cyclin A2, ATF2, MAPK phosphatase 1 (MKP1); PKCδ, Jun-D, Jun-B and c-Fos (Santa Cruz Biotechnology, Santa Cruz, CA); p-Akt (S473), p-Akt (T308), Akt, p-p70S6K1 (T389), p70S6K1, p-S6 ribosomal protein (S235/236), S6 ribosomal protein, p-c-Jun (S73), p-c-Jun (S63), c-Jun, glyceraldehyde 3-phosphate dehydrogenase (GAPDH), p-PKCδ (T505), p-p65 (S536), IκBα, p-MKP1 (S359), p-eIF4B (S422), eIF4B, p-mammalian target of rapamycin (mTOR) (S2448), mTOR, p-eEF2K (S366), eEF2K, p-eEF2 (T56), eukaryotic elongation factor 2 (eEF2), p-SEK1/mitogen-activated protein kinase kinase 4 (MKK4) (S257/T261), SEK1/MKK4, p-ATF2 (T71), HA-tag, JNK, p-JNK (T183/Y185), p38, p-p38 (T180/Y182), extracellular signal-regulated kinase (ERK) and p-ERK (T202/Y204) (Cell Signaling Technology, Beverly, MA); p-Jun-D (S255) (Abcam, Cambridge, UK) and horseradish peroxidase-conjugated secondary antibodies (PerkinElmer, Waltham, MA). .. Enhanced chemiluminescence detection reagents (Western Blot Chemiluminescence Reagent Plus; PerkinElmer) were used according to the manufacturers’ instructions to detect antigen–antibody complexes.

    Binding Assay:

    Article Title: Targeting the ERK signaling pathway as a potential treatment for insulin resistance and type 2 diabetes.
    Article Snippet: PD0325901 was obtained from SigmaAldrich (St. Louis, MO), and PD184352 was synthesized as described previously (37). .. Antibodies to phospho-ERK1/2 and to -actin were obtained from Sigma-Aldrich, those to ERK1/2, MAPK phosphatase-1 (MKP-1), PCNA, DLK (Pref-1), peroxisome proliferator-activated receptor (PPAR) , and CCAAT/enhancer binding protein (C/ EBP- ) were from Santa Cruz Biotechnology (Santa Cruz, CA), and those to adiponectin, mouse IL-6, and mouse TNF were from Abcam Address for reprint requests and other correspondence: M. Kohno, Laboratory of Cell Regulation, Dept. of Pharmaceutical Sciences, Graduate School of Biomedical Sciences, Nagasaki University, 1-14 Bunkyo-machi, Nagasaki 852-8521, Japan (e-mail: kohnom@nagasaki-u.ac.jp). ..



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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