nfatc inhibitor  (Cell Signaling Technology Inc)

 
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    Name:
    Cyclosporin A
    Description:
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    Catalog Number:
    9973
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    Category:
    Activators Inhibitors
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    Structured Review

    Cell Signaling Technology Inc nfatc inhibitor
    rBCG::PGL-I preferentially triggers <t>Syk/calcineurin/NFATc</t> through CR3 to rewire innate cells (A) DCs or PMNs from WT or myd88 −/− mice were infected with the three rBCG strains at MOI of 5. WT cells were treated with GS-9973 to inhibit the Syk pathway, or CsA to block NFATc translocation 1 h before infection. After overnight incubation supernatants were harvested to measure by ELISA IL-2 produced by DCs and IL-10 produced by PMNs. (B) Before infection of DCs or PMNs with rBCG::noPGL or rBCG::PGL-I as in (A) , cells were either incubated for 1 h with anti-CD11b antibody M1/70 to block CR3-mediated entry, or exposed to CsA to block NFATc translocation as indicated. IL-2 produced by DCs and IL-10 by PMNs after overnight incubation were measured by ELISA. Data are presented as mean ± SEM ( n = 4). * P
    Molecular Weight
    https://www.bioz.com/result/nfatc inhibitor/product/Cell Signaling Technology Inc
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    nfatc inhibitor - by Bioz Stars, 2020-09
    93/100 stars

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    1) Product Images from "CR3 Engaged by PGL-I Triggers Syk-Calcineurin-NFATc to Rewire the Innate Immune Response in Leprosy"

    Article Title: CR3 Engaged by PGL-I Triggers Syk-Calcineurin-NFATc to Rewire the Innate Immune Response in Leprosy

    Journal: Frontiers in Immunology

    doi: 10.3389/fimmu.2019.02913

    rBCG::PGL-I preferentially triggers Syk/calcineurin/NFATc through CR3 to rewire innate cells (A) DCs or PMNs from WT or myd88 −/− mice were infected with the three rBCG strains at MOI of 5. WT cells were treated with GS-9973 to inhibit the Syk pathway, or CsA to block NFATc translocation 1 h before infection. After overnight incubation supernatants were harvested to measure by ELISA IL-2 produced by DCs and IL-10 produced by PMNs. (B) Before infection of DCs or PMNs with rBCG::noPGL or rBCG::PGL-I as in (A) , cells were either incubated for 1 h with anti-CD11b antibody M1/70 to block CR3-mediated entry, or exposed to CsA to block NFATc translocation as indicated. IL-2 produced by DCs and IL-10 by PMNs after overnight incubation were measured by ELISA. Data are presented as mean ± SEM ( n = 4). * P
    Figure Legend Snippet: rBCG::PGL-I preferentially triggers Syk/calcineurin/NFATc through CR3 to rewire innate cells (A) DCs or PMNs from WT or myd88 −/− mice were infected with the three rBCG strains at MOI of 5. WT cells were treated with GS-9973 to inhibit the Syk pathway, or CsA to block NFATc translocation 1 h before infection. After overnight incubation supernatants were harvested to measure by ELISA IL-2 produced by DCs and IL-10 produced by PMNs. (B) Before infection of DCs or PMNs with rBCG::noPGL or rBCG::PGL-I as in (A) , cells were either incubated for 1 h with anti-CD11b antibody M1/70 to block CR3-mediated entry, or exposed to CsA to block NFATc translocation as indicated. IL-2 produced by DCs and IL-10 by PMNs after overnight incubation were measured by ELISA. Data are presented as mean ± SEM ( n = 4). * P

    Techniques Used: Mouse Assay, Infection, Blocking Assay, Translocation Assay, Incubation, Enzyme-linked Immunosorbent Assay, Produced

    CR3 triggers the Syk/calcineurin/NFATc pathway upon engagement by PGL-I-producing mycobacteria to rewire the innate response. rBCG::PGL-I targets the lectin domain of CR3 on the surface of DCs, PMNs, and MPs. Dectin-1 and CR3 cooperate to induce highly efficient entry of the bacilli. This triggers Syk for translocation of NFATc to the nucleus and initiates a transcriptional program to generate an NF-κB-independent mediator signature. This preferentially PGL-I-triggered pathway does not depend on MYD88 even though both cooperate to induce maximum levels of these mediators.
    Figure Legend Snippet: CR3 triggers the Syk/calcineurin/NFATc pathway upon engagement by PGL-I-producing mycobacteria to rewire the innate response. rBCG::PGL-I targets the lectin domain of CR3 on the surface of DCs, PMNs, and MPs. Dectin-1 and CR3 cooperate to induce highly efficient entry of the bacilli. This triggers Syk for translocation of NFATc to the nucleus and initiates a transcriptional program to generate an NF-κB-independent mediator signature. This preferentially PGL-I-triggered pathway does not depend on MYD88 even though both cooperate to induce maximum levels of these mediators.

    Techniques Used: Translocation Assay

    rBCG::PGL-I targeting CR3 triggers Syk and NFATc in vivo . (A,B) WT and itgam −/− mice were nasally infected with 5 × 10 6 CFUs of fluorescent rBCG::PGL-I or rBCG::noPGL, and received two nasal doses of Syk inhibitor GS-9973 administered 1 h before and after bacteria. BAL and lung tissues were harvested 24 h later to analyze cells by flow cytometry. (A,B) Numbers of Ly-6G + , CD11c − PMNs and Ly-6G − , CD11c + MPs harboring BCG-EGFP + recovered from the lung parenchyma from 11 individuals (A) or BAL from 12 individuals pooled per 2 (B) . (C) IL-10 produced in situ by lung cells was analyzed by ELISA in the first BAL from 12 individuals pooled per 2. (D) WT mice received two nasal doses of CsA 1 h before and 1 h after rBCG::PGL-I or rBCG::noPGL inhalation, to block NFATc translocation. IL-10 produced in situ by lung cells was analyzed as in (C) . Data are represented as individual values from n = 11 (A) or n = 6 (B–D) from two independent experiments. ** P
    Figure Legend Snippet: rBCG::PGL-I targeting CR3 triggers Syk and NFATc in vivo . (A,B) WT and itgam −/− mice were nasally infected with 5 × 10 6 CFUs of fluorescent rBCG::PGL-I or rBCG::noPGL, and received two nasal doses of Syk inhibitor GS-9973 administered 1 h before and after bacteria. BAL and lung tissues were harvested 24 h later to analyze cells by flow cytometry. (A,B) Numbers of Ly-6G + , CD11c − PMNs and Ly-6G − , CD11c + MPs harboring BCG-EGFP + recovered from the lung parenchyma from 11 individuals (A) or BAL from 12 individuals pooled per 2 (B) . (C) IL-10 produced in situ by lung cells was analyzed by ELISA in the first BAL from 12 individuals pooled per 2. (D) WT mice received two nasal doses of CsA 1 h before and 1 h after rBCG::PGL-I or rBCG::noPGL inhalation, to block NFATc translocation. IL-10 produced in situ by lung cells was analyzed as in (C) . Data are represented as individual values from n = 11 (A) or n = 6 (B–D) from two independent experiments. ** P

    Techniques Used: In Vivo, Mouse Assay, Infection, Flow Cytometry, Cytometry, Produced, In Situ, Enzyme-linked Immunosorbent Assay, Blocking Assay, Translocation Assay

    Related Articles

    Transfection:

    Article Title: FSH protects mouse granulosa cells from oxidative damage by repressing mitophagy
    Article Snippet: .. In some experiments, GCs were treated with 50 μM chloroquine (C6628; Sigma), 10 μM cyclosporine A (9973; Cell Signaling Technology), or 50 μM Z-VAD-FMK (S7023; Selleckchem) for 1, 2, or 3 h following incubation with H2 O2 for 1 h. For RNA interference, GCs were transfected with PINK1 siRNA (sc-44599; Santa Cruz) or scrambled control siRNA (sc-37007; Santa Cruz) for 24 h. After incubation with 200 μM H2 O2 for 0 or 1 h, the GCs were rinsed with PBS and cultured in serum-free medium with or without 7.5 IU/ml FSH for 2 h. ..

    Cell Culture:

    Article Title: FSH protects mouse granulosa cells from oxidative damage by repressing mitophagy
    Article Snippet: .. In some experiments, GCs were treated with 50 μM chloroquine (C6628; Sigma), 10 μM cyclosporine A (9973; Cell Signaling Technology), or 50 μM Z-VAD-FMK (S7023; Selleckchem) for 1, 2, or 3 h following incubation with H2 O2 for 1 h. For RNA interference, GCs were transfected with PINK1 siRNA (sc-44599; Santa Cruz) or scrambled control siRNA (sc-37007; Santa Cruz) for 24 h. After incubation with 200 μM H2 O2 for 0 or 1 h, the GCs were rinsed with PBS and cultured in serum-free medium with or without 7.5 IU/ml FSH for 2 h. ..

    Mouse Assay:

    Article Title: Evolutionarily conserved roles for blood-brain barrier xenobiotic transporters in endogenous steroid partitioning and behavior
    Article Snippet: .. Adult male FVB mice were injected with cyclosporin A (Cell Signaling 9973S; solubilized in 100% DMSO at 50mg/Kg body weight (bw)) or vehicle intraperitoneally at time zero (T=0). .. All mice were then injected with aldosterone (Sigma A9477; solubilized in 6.25% ethanol and 6.25% DMSO at 14mg/Kg bw) intravenously by tail vein at T=1hr.

    Incubation:

    Article Title: Hypoxic Preconditioning Attenuates Reoxygenation-Induced Skeletal Muscle Dysfunction in Aged Pulmonary TNF-α Overexpressing Mice
    Article Snippet: .. Muscle strips incubated with either diazoxide or cyclosporin A individually demonstrated improved contraction force comparable to the HPC curve (Figures , respectively). .. Diazoxide and cyclosporin A are potent mitoKATP channel opener and mPTP closer, respectively, which are both commonly used in studies investigating the signaling cascade underlying protection associated with ischemic preconditioning ( ; ; ).

    Article Title: FSH protects mouse granulosa cells from oxidative damage by repressing mitophagy
    Article Snippet: .. In some experiments, GCs were treated with 50 μM chloroquine (C6628; Sigma), 10 μM cyclosporine A (9973; Cell Signaling Technology), or 50 μM Z-VAD-FMK (S7023; Selleckchem) for 1, 2, or 3 h following incubation with H2 O2 for 1 h. For RNA interference, GCs were transfected with PINK1 siRNA (sc-44599; Santa Cruz) or scrambled control siRNA (sc-37007; Santa Cruz) for 24 h. After incubation with 200 μM H2 O2 for 0 or 1 h, the GCs were rinsed with PBS and cultured in serum-free medium with or without 7.5 IU/ml FSH for 2 h. ..

    other:

    Article Title: Evolutionarily conserved roles for blood-brain barrier xenobiotic transporters in endogenous steroid partitioning and behavior
    Article Snippet: The following conditions were compared: 1) vehicle followed by aldosterone, 2) cyclosporin A followed by aldosterone.

    Article Title: Hypoxic Preconditioning Attenuates Reoxygenation-Induced Skeletal Muscle Dysfunction in Aged Pulmonary TNF-α Overexpressing Mice
    Article Snippet: The results confirmed that the Tg+ muscles can be significantly strengthened during reoxygenation after treating with HPC (n = 5; p = 0.004 for the 1st contraction; p = 0.005 for the end contraction), diazoxide n = 5; p = 0.004 for the 1st contraction; p = 0.006 for the end contraction), or cyclosporin A (n = 5; p = 0.01 for the 1st contraction; p = 0.000 for the end contraction).

    Article Title: Hypoxic Preconditioning Attenuates Reoxygenation-Induced Skeletal Muscle Dysfunction in Aged Pulmonary TNF-α Overexpressing Mice
    Article Snippet: Similarly, our previous study using diazoxide or cyclosporin A reported that HPC protective effects involve the closure of mPTP and the opening of mitoKATP channels in wild-type muscles ( ).

    Article Title: Hypoxic Preconditioning Attenuates Reoxygenation-Induced Skeletal Muscle Dysfunction in Aged Pulmonary TNF-α Overexpressing Mice
    Article Snippet: Diazoxide and cyclosporin A are potent mitoKATP channel opener and mPTP closer, respectively, which are both commonly used in studies investigating the signaling cascade underlying protection associated with ischemic preconditioning ( ; ; ).

    Injection:

    Article Title: Evolutionarily conserved roles for blood-brain barrier xenobiotic transporters in endogenous steroid partitioning and behavior
    Article Snippet: .. Adult male FVB mice were injected with cyclosporin A (Cell Signaling 9973S; solubilized in 100% DMSO at 50mg/Kg body weight (bw)) or vehicle intraperitoneally at time zero (T=0). .. All mice were then injected with aldosterone (Sigma A9477; solubilized in 6.25% ethanol and 6.25% DMSO at 14mg/Kg bw) intravenously by tail vein at T=1hr.

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  • 93
    Cell Signaling Technology Inc nfatc inhibitor
    rBCG::PGL-I preferentially triggers <t>Syk/calcineurin/NFATc</t> through CR3 to rewire innate cells (A) DCs or PMNs from WT or myd88 −/− mice were infected with the three rBCG strains at MOI of 5. WT cells were treated with GS-9973 to inhibit the Syk pathway, or CsA to block NFATc translocation 1 h before infection. After overnight incubation supernatants were harvested to measure by ELISA IL-2 produced by DCs and IL-10 produced by PMNs. (B) Before infection of DCs or PMNs with rBCG::noPGL or rBCG::PGL-I as in (A) , cells were either incubated for 1 h with anti-CD11b antibody M1/70 to block CR3-mediated entry, or exposed to CsA to block NFATc translocation as indicated. IL-2 produced by DCs and IL-10 by PMNs after overnight incubation were measured by ELISA. Data are presented as mean ± SEM ( n = 4). * P
    Nfatc Inhibitor, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/nfatc inhibitor/product/Cell Signaling Technology Inc
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    nfatc inhibitor - by Bioz Stars, 2020-09
    93/100 stars
      Buy from Supplier

    Image Search Results


    rBCG::PGL-I preferentially triggers Syk/calcineurin/NFATc through CR3 to rewire innate cells (A) DCs or PMNs from WT or myd88 −/− mice were infected with the three rBCG strains at MOI of 5. WT cells were treated with GS-9973 to inhibit the Syk pathway, or CsA to block NFATc translocation 1 h before infection. After overnight incubation supernatants were harvested to measure by ELISA IL-2 produced by DCs and IL-10 produced by PMNs. (B) Before infection of DCs or PMNs with rBCG::noPGL or rBCG::PGL-I as in (A) , cells were either incubated for 1 h with anti-CD11b antibody M1/70 to block CR3-mediated entry, or exposed to CsA to block NFATc translocation as indicated. IL-2 produced by DCs and IL-10 by PMNs after overnight incubation were measured by ELISA. Data are presented as mean ± SEM ( n = 4). * P

    Journal: Frontiers in Immunology

    Article Title: CR3 Engaged by PGL-I Triggers Syk-Calcineurin-NFATc to Rewire the Innate Immune Response in Leprosy

    doi: 10.3389/fimmu.2019.02913

    Figure Lengend Snippet: rBCG::PGL-I preferentially triggers Syk/calcineurin/NFATc through CR3 to rewire innate cells (A) DCs or PMNs from WT or myd88 −/− mice were infected with the three rBCG strains at MOI of 5. WT cells were treated with GS-9973 to inhibit the Syk pathway, or CsA to block NFATc translocation 1 h before infection. After overnight incubation supernatants were harvested to measure by ELISA IL-2 produced by DCs and IL-10 produced by PMNs. (B) Before infection of DCs or PMNs with rBCG::noPGL or rBCG::PGL-I as in (A) , cells were either incubated for 1 h with anti-CD11b antibody M1/70 to block CR3-mediated entry, or exposed to CsA to block NFATc translocation as indicated. IL-2 produced by DCs and IL-10 by PMNs after overnight incubation were measured by ELISA. Data are presented as mean ± SEM ( n = 4). * P

    Article Snippet: Mice received 40 μL of vehicle (DMSO 2%), or 1 μM Syk inhibitor (GS-9973, ApexBio Technology), or 50 ng/ml NFATc inhibitor (Cyclosporin A, Cell signaling Technology) via the nasal route 1 h before and 1 h after BCG infection.

    Techniques: Mouse Assay, Infection, Blocking Assay, Translocation Assay, Incubation, Enzyme-linked Immunosorbent Assay, Produced

    CR3 triggers the Syk/calcineurin/NFATc pathway upon engagement by PGL-I-producing mycobacteria to rewire the innate response. rBCG::PGL-I targets the lectin domain of CR3 on the surface of DCs, PMNs, and MPs. Dectin-1 and CR3 cooperate to induce highly efficient entry of the bacilli. This triggers Syk for translocation of NFATc to the nucleus and initiates a transcriptional program to generate an NF-κB-independent mediator signature. This preferentially PGL-I-triggered pathway does not depend on MYD88 even though both cooperate to induce maximum levels of these mediators.

    Journal: Frontiers in Immunology

    Article Title: CR3 Engaged by PGL-I Triggers Syk-Calcineurin-NFATc to Rewire the Innate Immune Response in Leprosy

    doi: 10.3389/fimmu.2019.02913

    Figure Lengend Snippet: CR3 triggers the Syk/calcineurin/NFATc pathway upon engagement by PGL-I-producing mycobacteria to rewire the innate response. rBCG::PGL-I targets the lectin domain of CR3 on the surface of DCs, PMNs, and MPs. Dectin-1 and CR3 cooperate to induce highly efficient entry of the bacilli. This triggers Syk for translocation of NFATc to the nucleus and initiates a transcriptional program to generate an NF-κB-independent mediator signature. This preferentially PGL-I-triggered pathway does not depend on MYD88 even though both cooperate to induce maximum levels of these mediators.

    Article Snippet: Mice received 40 μL of vehicle (DMSO 2%), or 1 μM Syk inhibitor (GS-9973, ApexBio Technology), or 50 ng/ml NFATc inhibitor (Cyclosporin A, Cell signaling Technology) via the nasal route 1 h before and 1 h after BCG infection.

    Techniques: Translocation Assay

    rBCG::PGL-I targeting CR3 triggers Syk and NFATc in vivo . (A,B) WT and itgam −/− mice were nasally infected with 5 × 10 6 CFUs of fluorescent rBCG::PGL-I or rBCG::noPGL, and received two nasal doses of Syk inhibitor GS-9973 administered 1 h before and after bacteria. BAL and lung tissues were harvested 24 h later to analyze cells by flow cytometry. (A,B) Numbers of Ly-6G + , CD11c − PMNs and Ly-6G − , CD11c + MPs harboring BCG-EGFP + recovered from the lung parenchyma from 11 individuals (A) or BAL from 12 individuals pooled per 2 (B) . (C) IL-10 produced in situ by lung cells was analyzed by ELISA in the first BAL from 12 individuals pooled per 2. (D) WT mice received two nasal doses of CsA 1 h before and 1 h after rBCG::PGL-I or rBCG::noPGL inhalation, to block NFATc translocation. IL-10 produced in situ by lung cells was analyzed as in (C) . Data are represented as individual values from n = 11 (A) or n = 6 (B–D) from two independent experiments. ** P

    Journal: Frontiers in Immunology

    Article Title: CR3 Engaged by PGL-I Triggers Syk-Calcineurin-NFATc to Rewire the Innate Immune Response in Leprosy

    doi: 10.3389/fimmu.2019.02913

    Figure Lengend Snippet: rBCG::PGL-I targeting CR3 triggers Syk and NFATc in vivo . (A,B) WT and itgam −/− mice were nasally infected with 5 × 10 6 CFUs of fluorescent rBCG::PGL-I or rBCG::noPGL, and received two nasal doses of Syk inhibitor GS-9973 administered 1 h before and after bacteria. BAL and lung tissues were harvested 24 h later to analyze cells by flow cytometry. (A,B) Numbers of Ly-6G + , CD11c − PMNs and Ly-6G − , CD11c + MPs harboring BCG-EGFP + recovered from the lung parenchyma from 11 individuals (A) or BAL from 12 individuals pooled per 2 (B) . (C) IL-10 produced in situ by lung cells was analyzed by ELISA in the first BAL from 12 individuals pooled per 2. (D) WT mice received two nasal doses of CsA 1 h before and 1 h after rBCG::PGL-I or rBCG::noPGL inhalation, to block NFATc translocation. IL-10 produced in situ by lung cells was analyzed as in (C) . Data are represented as individual values from n = 11 (A) or n = 6 (B–D) from two independent experiments. ** P

    Article Snippet: Mice received 40 μL of vehicle (DMSO 2%), or 1 μM Syk inhibitor (GS-9973, ApexBio Technology), or 50 ng/ml NFATc inhibitor (Cyclosporin A, Cell signaling Technology) via the nasal route 1 h before and 1 h after BCG infection.

    Techniques: In Vivo, Mouse Assay, Infection, Flow Cytometry, Cytometry, Produced, In Situ, Enzyme-linked Immunosorbent Assay, Blocking Assay, Translocation Assay