jak inhibitor  (Millipore)

 
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  • 92
    Name:
    Methyl 3 indoleglyoxylate
    Description:

    Catalog Number:
    515213
    Price:
    None
    Applications:
    . Reactant for preparation of sotrastaurin analogs as protein kinase inhibitors. Reactant for synthesis of GSK-3 inhibitors. Reactant for Diels-Alder cycloaddition. Reactant for preparation of a Janus kinase 3 inhibitor. Reactant for synthesis of cephalandole alkaloids. Reactant for stereoselective preparation of COX-2 inhibitor as anticancer agent. Reactant for synthesis of cycloalkene indole carbazole alkaloids via ring-closing metathesis
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    Structured Review

    Millipore jak inhibitor
    Methyl 3 indoleglyoxylate

    https://www.bioz.com/result/jak inhibitor/product/Millipore
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    jak inhibitor - by Bioz Stars, 2021-04
    92/100 stars

    Images

    1) Product Images from "IL‐7 induces sCD127 release and mCD127 downregulation in human CD8+ T cells by distinct yet overlapping mechanisms, both of which are impaired in HIV infection"

    Article Title: IL‐7 induces sCD127 release and mCD127 downregulation in human CD8+ T cells by distinct yet overlapping mechanisms, both of which are impaired in HIV infection

    Journal: European Journal of Immunology

    doi: 10.1002/eji.201948453

    IL‐7‐induced downregulation of mCD127 is dependent on JAK and PI3K but not STAT5. CD8 + T cells were magnetically isolated from PBMCs derived from healthy individuals and cultured with or without IL‐7. For some experiments, inhibitors were used as described. Flow cytometry was performed to evaluate expression of CD127. (A) Representative flow cytometry histogram showing the CD127 median fluorescence intensity (MFI) and the percentage of CD127 + cells among unstained cells (light gray), medium control (dark gray), and the IL‐7‐ (10 ng/mL) treated cells (black unfilled). The gating strategy is shown in Supporting Information Fig. S6. (B) Time course of CD127 expression on CD8 + cells with media control (dotted line), 1 ng/mL IL‐7 (gray line), and 10 ng/mL IL‐7 (black line). Significance was calculated between each IL‐7 concentration in relation to the medium control (* p
    Figure Legend Snippet: IL‐7‐induced downregulation of mCD127 is dependent on JAK and PI3K but not STAT5. CD8 + T cells were magnetically isolated from PBMCs derived from healthy individuals and cultured with or without IL‐7. For some experiments, inhibitors were used as described. Flow cytometry was performed to evaluate expression of CD127. (A) Representative flow cytometry histogram showing the CD127 median fluorescence intensity (MFI) and the percentage of CD127 + cells among unstained cells (light gray), medium control (dark gray), and the IL‐7‐ (10 ng/mL) treated cells (black unfilled). The gating strategy is shown in Supporting Information Fig. S6. (B) Time course of CD127 expression on CD8 + cells with media control (dotted line), 1 ng/mL IL‐7 (gray line), and 10 ng/mL IL‐7 (black line). Significance was calculated between each IL‐7 concentration in relation to the medium control (* p

    Techniques Used: Isolation, Derivative Assay, Cell Culture, Flow Cytometry, Expressing, Fluorescence, Concentration Assay

    IL‐7‐induced sCD127 release from CD8 + T cells involves JAK, STAT5, and PI3K. CD8 + T cells were magnetically isolated from PBMCs derived from healthy individuals and cultured with or without IL‐7. For some experiments, inhibitors were used as described. ELISA assays were performed to evaluate secretion of sCD127. (A) sCD127 release with media alone (dotted line), 1 ng/mL IL‐7 (gray line), and 10 ng/mL IL‐7 (black line) over time. sCD127 release was compared in the different time points between media alone and 1 ng/mL IL‐7 or media alone and 10 ng/mL IL‐7 (two‐way ANOVA with Bonferroni posttest); between 1 ng/mL IL‐7 and 10 ng/mL IL‐7 on each time point (two‐way ANOVA with Bonferroni posttest); and between the time points in the media alone (one‐way ANOVA with Bonferroni post‐test), n = 4. Data are shown as mean ± SEM of four samples from two independent experiments. (B) sCD127 release was normalized to the control values (values obtained in the media alone cell cultures were subtracted) and compared between cells treated with 1 ng/mL IL‐7 (grey line) or 10 ng/mL IL‐7 (black line) over time (two‐way ANOVA with Bonferroni posttest), n = 4. Data are shown as mean ± SEM of four samples from two independent experiments. (C) The impact of JAK inhibitor (10 μM), (D) STAT5 inhibitor (250 μM), and (E) PI3K (25 μM) inhibitor in the IL‐7‐induced sCD127 secretion in 48 h (paired t test), n = 7. Graphs show the distribution of seven samples from four independent experiments. The dotted line represents the limit of detection for this assay (125 pg/mL) (* p
    Figure Legend Snippet: IL‐7‐induced sCD127 release from CD8 + T cells involves JAK, STAT5, and PI3K. CD8 + T cells were magnetically isolated from PBMCs derived from healthy individuals and cultured with or without IL‐7. For some experiments, inhibitors were used as described. ELISA assays were performed to evaluate secretion of sCD127. (A) sCD127 release with media alone (dotted line), 1 ng/mL IL‐7 (gray line), and 10 ng/mL IL‐7 (black line) over time. sCD127 release was compared in the different time points between media alone and 1 ng/mL IL‐7 or media alone and 10 ng/mL IL‐7 (two‐way ANOVA with Bonferroni posttest); between 1 ng/mL IL‐7 and 10 ng/mL IL‐7 on each time point (two‐way ANOVA with Bonferroni posttest); and between the time points in the media alone (one‐way ANOVA with Bonferroni post‐test), n = 4. Data are shown as mean ± SEM of four samples from two independent experiments. (B) sCD127 release was normalized to the control values (values obtained in the media alone cell cultures were subtracted) and compared between cells treated with 1 ng/mL IL‐7 (grey line) or 10 ng/mL IL‐7 (black line) over time (two‐way ANOVA with Bonferroni posttest), n = 4. Data are shown as mean ± SEM of four samples from two independent experiments. (C) The impact of JAK inhibitor (10 μM), (D) STAT5 inhibitor (250 μM), and (E) PI3K (25 μM) inhibitor in the IL‐7‐induced sCD127 secretion in 48 h (paired t test), n = 7. Graphs show the distribution of seven samples from four independent experiments. The dotted line represents the limit of detection for this assay (125 pg/mL) (* p

    Techniques Used: Isolation, Derivative Assay, Cell Culture, Enzyme-linked Immunosorbent Assay

    2) Product Images from "Autocrine Regulation of Pulmonary Inflammation by Effector T-Cell Derived IL-10 during Infection with Respiratory Syncytial Virus"

    Article Title: Autocrine Regulation of Pulmonary Inflammation by Effector T-Cell Derived IL-10 during Infection with Respiratory Syncytial Virus

    Journal: PLoS Pathogens

    doi: 10.1371/journal.ppat.1002173

    Autocrine regulation of pulmonary inflammation by effector T cell-derived IL-10 during RSV infection. (A, B). BALB/c mice were infected with RSV. At d7 p.i., Lung CD8 + cells were purified and stimulated as indicated in vitro . (A) CD8 + T cells were stimulated with rIL-10 in the absence or presence of JAK inhibitor. STAT3 phophorylation was determined by ICS. (B) CD8 + T cells were left un-stimulated or stimulated with plate-bound a-CD3 overnight in the absence or presence of rIL-10 or rIL-10 plus α-IL-10R. IFN-γ release to the medium was determined by ELISA. (C – F) IL-10Rα fl/fl mice or CD4-Cre + IL-10Rα fl/fl mice were infected with RSV. (C) The expression of IL-10Rα in lung monocytes, NK cells, CD4 + and CD8 + T cells at d6 post infection was determined by flow cytometry. (D) IFN-γ levels in the BALF were determined by ELISA. P value was determined by unpaired two-tailed Student t test. * indicates P
    Figure Legend Snippet: Autocrine regulation of pulmonary inflammation by effector T cell-derived IL-10 during RSV infection. (A, B). BALB/c mice were infected with RSV. At d7 p.i., Lung CD8 + cells were purified and stimulated as indicated in vitro . (A) CD8 + T cells were stimulated with rIL-10 in the absence or presence of JAK inhibitor. STAT3 phophorylation was determined by ICS. (B) CD8 + T cells were left un-stimulated or stimulated with plate-bound a-CD3 overnight in the absence or presence of rIL-10 or rIL-10 plus α-IL-10R. IFN-γ release to the medium was determined by ELISA. (C – F) IL-10Rα fl/fl mice or CD4-Cre + IL-10Rα fl/fl mice were infected with RSV. (C) The expression of IL-10Rα in lung monocytes, NK cells, CD4 + and CD8 + T cells at d6 post infection was determined by flow cytometry. (D) IFN-γ levels in the BALF were determined by ELISA. P value was determined by unpaired two-tailed Student t test. * indicates P

    Techniques Used: Derivative Assay, Infection, Mouse Assay, Purification, In Vitro, Enzyme-linked Immunosorbent Assay, Expressing, Flow Cytometry, Cytometry, Two Tailed Test

    3) Product Images from "Oncostatin M decreases interleukin-1 β secretion by human synovial fibroblasts and attenuates an acute inflammatory reaction in vivo"

    Article Title: Oncostatin M decreases interleukin-1 β secretion by human synovial fibroblasts and attenuates an acute inflammatory reaction in vivo

    Journal: Journal of Cellular and Molecular Medicine

    doi: 10.1111/j.1582-4934.2011.01412.x

    Signalling pathways mediating the OSM-effects on the IL-1β, CXCL8, IL-6 and CCL2 expression in stimulated HSFs. (A) HSFs were stimulated or not with a combination of LPS and GM-CSF for 10 min. in the absence or presence of OSM (10 ng/ml) and its neutralizing antibody (10 μg/ml), as indicated, prior to lysis and subsequent immunoblot analysis using primary antibodies raised against phospho-ERK1/2, phospho-STAT-1 (Tyr 701) and total STAT-1 (as a loading control). Immunoblots shown are representative of three independent experiments; bands were quantified by densitometric analysis and results presented as mean ± S.E.M. When indicated, cells were pre-incubated for 15 min. with the MEK inhibitor U0126 (10 μM) or the Jak inhibitor (0.5 μM) before stimulation in the presence of OSM. * P
    Figure Legend Snippet: Signalling pathways mediating the OSM-effects on the IL-1β, CXCL8, IL-6 and CCL2 expression in stimulated HSFs. (A) HSFs were stimulated or not with a combination of LPS and GM-CSF for 10 min. in the absence or presence of OSM (10 ng/ml) and its neutralizing antibody (10 μg/ml), as indicated, prior to lysis and subsequent immunoblot analysis using primary antibodies raised against phospho-ERK1/2, phospho-STAT-1 (Tyr 701) and total STAT-1 (as a loading control). Immunoblots shown are representative of three independent experiments; bands were quantified by densitometric analysis and results presented as mean ± S.E.M. When indicated, cells were pre-incubated for 15 min. with the MEK inhibitor U0126 (10 μM) or the Jak inhibitor (0.5 μM) before stimulation in the presence of OSM. * P

    Techniques Used: Expressing, Lysis, Western Blot, Incubation

    4) Product Images from "Glucocorticoids potentiate IL-6-induced SP-B expression in H441 cells by enhancing the JAK-STAT signaling pathway"

    Article Title: Glucocorticoids potentiate IL-6-induced SP-B expression in H441 cells by enhancing the JAK-STAT signaling pathway

    Journal: American Journal of Physiology - Lung Cellular and Molecular Physiology

    doi: 10.1152/ajplung.00055.2010

    Effect of a JAK inhibitor on the synergistic effect of glucocorticoids and IL-6 on SP-B mRNA expression. H441 cells were incubated with IL-6 or DXM alone for 48 h or a combination of IL-6 with DXM for 48 h. Subsequent incubation with a JAK inhibitor significantly
    Figure Legend Snippet: Effect of a JAK inhibitor on the synergistic effect of glucocorticoids and IL-6 on SP-B mRNA expression. H441 cells were incubated with IL-6 or DXM alone for 48 h or a combination of IL-6 with DXM for 48 h. Subsequent incubation with a JAK inhibitor significantly

    Techniques Used: Expressing, Incubation

    Effect of JAK inhibition on the glucocorticoid effect on IL-6-induced STAT3 phosphorylation. H441 cells were incubated with IL-6 and DXM alone or a combination of IL-6 and DXM. Subsequent incubation with a JAK inhibitor significantly reduced the effect
    Figure Legend Snippet: Effect of JAK inhibition on the glucocorticoid effect on IL-6-induced STAT3 phosphorylation. H441 cells were incubated with IL-6 and DXM alone or a combination of IL-6 and DXM. Subsequent incubation with a JAK inhibitor significantly reduced the effect

    Techniques Used: Inhibition, Incubation

    Related Articles

    Cell Culture:

    Article Title: Human foreskin fibroblast produces interleukin-6 to support derivation and self-renewal of mouse embryonic stem cells
    Article Snippet: The derivation and culture medium was DMEM (Gibco) with 10% fetal bovine serum, 100 U/ml penicillin, 100 μg/ml streptomycin, 0.1 mM β-mercaptoethanol (Sigma, St. Louis, MO, USA) and 2 mM L -glutamine. .. To determine the effect of the JAK pathway, 10 or 20 μM JAK inhibitor (Calbiochem, Darmstadt, Bundesland, Germany) was added to the cell culture to inhibit the phosphorylation of Stat3. .. Alkaline phosphatase staining ESC colonies were fixed with 4% paraformaldehyde and permeabilized by 0.1% Triton X-100 in PBS.

    other:

    Article Title: Apoptosis induced by JAK2 inhibition is mediated by Bim and enhanced by the BH3 mimetic ABT-737 in JAK2 mutant human erythroid cells
    Article Snippet: JAK inhibitor I was purchased from Calbiochem.

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  • 85
    Millipore jak2 inhibitors ii
    AGK enhances <t>JAK2</t> activity by blocking JH2-mediated autoinhibition of JAK2.
    Jak2 Inhibitors Ii, supplied by Millipore, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/jak2 inhibitors ii/product/Millipore
    Average 85 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    jak2 inhibitors ii - by Bioz Stars, 2021-04
    85/100 stars
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    94
    Millipore jak inhibitor i
    Effects of alterations in Jak-Stat pathway on PrPres formation. (A) Immunoblotting of PrPres in N167 cells treated with Jak inhibitor. Cells were treated with Jak <t>inhibitor</t> I at the indicated doses for 3 days. The amount of DMSO was equilibrated in all
    Jak Inhibitor I, supplied by Millipore, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/jak inhibitor i/product/Millipore
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    jak inhibitor i - by Bioz Stars, 2021-04
    94/100 stars
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    96
    Millipore jak2 inhibitor
    Effect of ApoE on β-cells is dependent on JAK/STAT signaling. A) List of upregulated proteins from the phospho explorer array from ApoE-treated whole islets in adherence compared to controls. Fold changes are considered significant when they are greater than 1.5. The results of the Antibody Array Assay identified STAT3 (phosphorylated at Ser727) as the most-upregulated protein. <t>JAK2</t> (phosphorylated at Tyr221) was also among the most upregulated proteins. B) Left, Western blot analysis of phosphorylated STAT3 and JAK2, confirming the array results showing a nearly two-fold increase in the ApoE treated islets at day 14. Right, quantification of bands using Image J software. C) Western blot analysis using STAT3 and JAK2 inhibitors, which demonstrates that these inhibitors can inhibit the phosphorylation of these proteins in whole adhered islets at day 14 with or without ApoE. D) Gene expression analysis of whole adhered pancreatic islets cultured for 14 days with ApoE as well as STAT3 and Jak2 inhibitors. As expected, ApoE treatment significantly increased β-cell gene expression relative to controls, while this increase was abolished in islets treated with STAT3 and JAK2 inhibitors. Data presented as mean ± SEM, where p
    Jak2 Inhibitor, supplied by Millipore, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/jak2 inhibitor/product/Millipore
    Average 96 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    jak2 inhibitor - by Bioz Stars, 2021-04
    96/100 stars
      Buy from Supplier

    Image Search Results


    AGK enhances JAK2 activity by blocking JH2-mediated autoinhibition of JAK2.

    Journal: The Journal of Clinical Investigation

    Article Title: Acylglycerol kinase augments JAK2/STAT3 signaling in esophageal squamous cells

    doi: 10.1172/JCI68143

    Figure Lengend Snippet: AGK enhances JAK2 activity by blocking JH2-mediated autoinhibition of JAK2.

    Article Snippet: JAK2 inhibitors II and III (SD-1029) were purchased from Millipore.

    Techniques: Activity Assay, Blocking Assay

    Silencing JAK2 reverses the CSC-promoting effect of AGK.

    Journal: The Journal of Clinical Investigation

    Article Title: Acylglycerol kinase augments JAK2/STAT3 signaling in esophageal squamous cells

    doi: 10.1172/JCI68143

    Figure Lengend Snippet: Silencing JAK2 reverses the CSC-promoting effect of AGK.

    Article Snippet: JAK2 inhibitors II and III (SD-1029) were purchased from Millipore.

    Techniques:

    JAK2/STAT3 signaling is required for the cancer stem cell–promoting effect of AGK.

    Journal: The Journal of Clinical Investigation

    Article Title: Acylglycerol kinase augments JAK2/STAT3 signaling in esophageal squamous cells

    doi: 10.1172/JCI68143

    Figure Lengend Snippet: JAK2/STAT3 signaling is required for the cancer stem cell–promoting effect of AGK.

    Article Snippet: JAK2 inhibitors II and III (SD-1029) were purchased from Millipore.

    Techniques:

    Identification of AGK as a JH2 domain–interacting protein that activates the JAK2/STAT3 pathway.

    Journal: The Journal of Clinical Investigation

    Article Title: Acylglycerol kinase augments JAK2/STAT3 signaling in esophageal squamous cells

    doi: 10.1172/JCI68143

    Figure Lengend Snippet: Identification of AGK as a JH2 domain–interacting protein that activates the JAK2/STAT3 pathway.

    Article Snippet: JAK2 inhibitors II and III (SD-1029) were purchased from Millipore.

    Techniques:

    Effects of alterations in Jak-Stat pathway on PrPres formation. (A) Immunoblotting of PrPres in N167 cells treated with Jak inhibitor. Cells were treated with Jak inhibitor I at the indicated doses for 3 days. The amount of DMSO was equilibrated in all

    Journal: Journal of Virology

    Article Title: Efficacy and Mechanism of a Glycoside Compound Inhibiting Abnormal Prion Protein Formation in Prion-Infected Cells: Implications of Interferon and Phosphodiesterase 4D-Interacting Protein

    doi: 10.1128/JVI.03775-13

    Figure Lengend Snippet: Effects of alterations in Jak-Stat pathway on PrPres formation. (A) Immunoblotting of PrPres in N167 cells treated with Jak inhibitor. Cells were treated with Jak inhibitor I at the indicated doses for 3 days. The amount of DMSO was equilibrated in all

    Article Snippet: A Janus activated kinase inhibitor, Jak inhibitor I, was purchased from Calbiochem Corp. (La Jolla, CA) and dissolved in DMSO.

    Techniques:

    Effect of ApoE on β-cells is dependent on JAK/STAT signaling. A) List of upregulated proteins from the phospho explorer array from ApoE-treated whole islets in adherence compared to controls. Fold changes are considered significant when they are greater than 1.5. The results of the Antibody Array Assay identified STAT3 (phosphorylated at Ser727) as the most-upregulated protein. JAK2 (phosphorylated at Tyr221) was also among the most upregulated proteins. B) Left, Western blot analysis of phosphorylated STAT3 and JAK2, confirming the array results showing a nearly two-fold increase in the ApoE treated islets at day 14. Right, quantification of bands using Image J software. C) Western blot analysis using STAT3 and JAK2 inhibitors, which demonstrates that these inhibitors can inhibit the phosphorylation of these proteins in whole adhered islets at day 14 with or without ApoE. D) Gene expression analysis of whole adhered pancreatic islets cultured for 14 days with ApoE as well as STAT3 and Jak2 inhibitors. As expected, ApoE treatment significantly increased β-cell gene expression relative to controls, while this increase was abolished in islets treated with STAT3 and JAK2 inhibitors. Data presented as mean ± SEM, where p

    Journal: PLoS ONE

    Article Title: Apolipoprotein E is a pancreatic extracellular factor that maintains mature β-cell gene expression

    doi: 10.1371/journal.pone.0204595

    Figure Lengend Snippet: Effect of ApoE on β-cells is dependent on JAK/STAT signaling. A) List of upregulated proteins from the phospho explorer array from ApoE-treated whole islets in adherence compared to controls. Fold changes are considered significant when they are greater than 1.5. The results of the Antibody Array Assay identified STAT3 (phosphorylated at Ser727) as the most-upregulated protein. JAK2 (phosphorylated at Tyr221) was also among the most upregulated proteins. B) Left, Western blot analysis of phosphorylated STAT3 and JAK2, confirming the array results showing a nearly two-fold increase in the ApoE treated islets at day 14. Right, quantification of bands using Image J software. C) Western blot analysis using STAT3 and JAK2 inhibitors, which demonstrates that these inhibitors can inhibit the phosphorylation of these proteins in whole adhered islets at day 14 with or without ApoE. D) Gene expression analysis of whole adhered pancreatic islets cultured for 14 days with ApoE as well as STAT3 and Jak2 inhibitors. As expected, ApoE treatment significantly increased β-cell gene expression relative to controls, while this increase was abolished in islets treated with STAT3 and JAK2 inhibitors. Data presented as mean ± SEM, where p

    Article Snippet: Cells were treated with either 1–2 μg/mL human recombinant ApoE (R & D systems), 20 uM JAK2 inhibitor (Tyrphostin AG490, Sigma), 2.5 uM STAT3 inhibitor (Pp-YLKTK-mts, Millipore), 20 ug LDL Receptor Blocking Peptide (Cayman Chemical), 50 mg of Cholesterol in 1 g of methyl β-cyclodextrin (Sigma), 22R-Hydroxycholesterol 10 uM (Sigma), Simvastatin 1uM (Sigma), 2 units/ml of Heparinase III (Sigma) and 500 uM Palmitate (Sigma).

    Techniques: Ab Array, Western Blot, Software, Expressing, Cell Culture