ptdins  (Echelon Biosciences)


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    Structured Review

    Echelon Biosciences ptdins
    JAK2 inhibition dysregulates signaling networks during Th17 polarization. A , primary murine CD4 + T cells were activated for 10 min with constant amounts of anti-CD3 antibody, soluble anti-CD28 antibody, and TGF-β with varying amounts of IL-6. Immunoblotting was performed for p-ZAP7(Y319) and total ZAP70. Densitometry was performed on immunoblots across three biological replicates. Shown are mean ± SD. Primary murine CD4 + T cells were activated under Th17 (TCR+TGF-β+IL-6) or Treg polarization conditions (TCR+TGF-β) for 10 min in the presence or absence of 200 nM JAK2 inhibitor. B , immunoblotting was performed for p-ZAP7(Y319), ZAP70, p-CSK-S364, and CSK. Densitometry was performed on immunoblots across three biological replicates from panel B to determine the relative amount of ( C ) p-CSK-S364 and ( D ) p-ZAP70(Y319) normalized to total CSK and Zap70 abundance respectively. Shown are mean ± SD; p values were calculated by one-way ANOVA. E , primary murine CD4 + T cells were activated under Th17 (TCR+ TGF-β+IL-6) or Treg polarization conditions (TCR+ TGF-β) for 10 min in the presence or absence of 200 nM JAK2 inhibitor. Immunoblotting was performed for p-P85 (Y458) and P85. F , densitometry was performed on immunoblots across three biological replicates from panel E were p-P85(Y458) was normalized to total P85. Shown are mean ± SD; p values were calculated by one-way ANOVA. Mass ELISA assays were utilized to determine the relative level of ( G ) <t>PtdIns(3,4,5)P3,</t> and ( H ) PtdIns(4,5)P2 generated in primary murine CD4 + T cells activated under Th17 or Treg polarization conditions for 10 min in the presence or absence of the JAK2 inhibitor. Shown are mean ± SD from three biological replicates; p values were calculated by one-way ANOVA. I , primary murine CD4 + T cells were activated for 10 min with constant amounts of anti-CD3 antibody, anti-CD28 antibody, and TGF-β with varying amounts of IL-6. Immunoblotting was performed for p-AKT(S473) and total AKT. Densitometry was performed on immunoblots across three biological replicates. Shown are mean ± SD. Source data are provided for the immunoblots in panels A , B , E , and I .
    Ptdins, supplied by Echelon Biosciences, 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/ptdins/product/Echelon Biosciences
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
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    1) Product Images from "Synergistic and additive interactions between receptor signaling networks drive the regulatory T cell versus T helper 17 cell fate choice"

    Article Title: Synergistic and additive interactions between receptor signaling networks drive the regulatory T cell versus T helper 17 cell fate choice

    Journal: The Journal of Biological Chemistry

    doi: 10.1016/j.jbc.2021.101330

    JAK2 inhibition dysregulates signaling networks during Th17 polarization. A , primary murine CD4 + T cells were activated for 10 min with constant amounts of anti-CD3 antibody, soluble anti-CD28 antibody, and TGF-β with varying amounts of IL-6. Immunoblotting was performed for p-ZAP7(Y319) and total ZAP70. Densitometry was performed on immunoblots across three biological replicates. Shown are mean ± SD. Primary murine CD4 + T cells were activated under Th17 (TCR+TGF-β+IL-6) or Treg polarization conditions (TCR+TGF-β) for 10 min in the presence or absence of 200 nM JAK2 inhibitor. B , immunoblotting was performed for p-ZAP7(Y319), ZAP70, p-CSK-S364, and CSK. Densitometry was performed on immunoblots across three biological replicates from panel B to determine the relative amount of ( C ) p-CSK-S364 and ( D ) p-ZAP70(Y319) normalized to total CSK and Zap70 abundance respectively. Shown are mean ± SD; p values were calculated by one-way ANOVA. E , primary murine CD4 + T cells were activated under Th17 (TCR+ TGF-β+IL-6) or Treg polarization conditions (TCR+ TGF-β) for 10 min in the presence or absence of 200 nM JAK2 inhibitor. Immunoblotting was performed for p-P85 (Y458) and P85. F , densitometry was performed on immunoblots across three biological replicates from panel E were p-P85(Y458) was normalized to total P85. Shown are mean ± SD; p values were calculated by one-way ANOVA. Mass ELISA assays were utilized to determine the relative level of ( G ) PtdIns(3,4,5)P3, and ( H ) PtdIns(4,5)P2 generated in primary murine CD4 + T cells activated under Th17 or Treg polarization conditions for 10 min in the presence or absence of the JAK2 inhibitor. Shown are mean ± SD from three biological replicates; p values were calculated by one-way ANOVA. I , primary murine CD4 + T cells were activated for 10 min with constant amounts of anti-CD3 antibody, anti-CD28 antibody, and TGF-β with varying amounts of IL-6. Immunoblotting was performed for p-AKT(S473) and total AKT. Densitometry was performed on immunoblots across three biological replicates. Shown are mean ± SD. Source data are provided for the immunoblots in panels A , B , E , and I .
    Figure Legend Snippet: JAK2 inhibition dysregulates signaling networks during Th17 polarization. A , primary murine CD4 + T cells were activated for 10 min with constant amounts of anti-CD3 antibody, soluble anti-CD28 antibody, and TGF-β with varying amounts of IL-6. Immunoblotting was performed for p-ZAP7(Y319) and total ZAP70. Densitometry was performed on immunoblots across three biological replicates. Shown are mean ± SD. Primary murine CD4 + T cells were activated under Th17 (TCR+TGF-β+IL-6) or Treg polarization conditions (TCR+TGF-β) for 10 min in the presence or absence of 200 nM JAK2 inhibitor. B , immunoblotting was performed for p-ZAP7(Y319), ZAP70, p-CSK-S364, and CSK. Densitometry was performed on immunoblots across three biological replicates from panel B to determine the relative amount of ( C ) p-CSK-S364 and ( D ) p-ZAP70(Y319) normalized to total CSK and Zap70 abundance respectively. Shown are mean ± SD; p values were calculated by one-way ANOVA. E , primary murine CD4 + T cells were activated under Th17 (TCR+ TGF-β+IL-6) or Treg polarization conditions (TCR+ TGF-β) for 10 min in the presence or absence of 200 nM JAK2 inhibitor. Immunoblotting was performed for p-P85 (Y458) and P85. F , densitometry was performed on immunoblots across three biological replicates from panel E were p-P85(Y458) was normalized to total P85. Shown are mean ± SD; p values were calculated by one-way ANOVA. Mass ELISA assays were utilized to determine the relative level of ( G ) PtdIns(3,4,5)P3, and ( H ) PtdIns(4,5)P2 generated in primary murine CD4 + T cells activated under Th17 or Treg polarization conditions for 10 min in the presence or absence of the JAK2 inhibitor. Shown are mean ± SD from three biological replicates; p values were calculated by one-way ANOVA. I , primary murine CD4 + T cells were activated for 10 min with constant amounts of anti-CD3 antibody, anti-CD28 antibody, and TGF-β with varying amounts of IL-6. Immunoblotting was performed for p-AKT(S473) and total AKT. Densitometry was performed on immunoblots across three biological replicates. Shown are mean ± SD. Source data are provided for the immunoblots in panels A , B , E , and I .

    Techniques Used: Inhibition, Western Blot, Enzyme-linked Immunosorbent Assay, Generated

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    Echelon Biosciences biotinylated anti ptdins 4 5 p2 igm
    JAK2 inhibition dysregulates signaling networks during Th17 polarization. A , primary murine CD4 + T cells were activated for 10 min with constant amounts of <t>anti-CD3</t> antibody, soluble anti-CD28 antibody, and TGF-β with varying amounts of IL-6. Immunoblotting was performed for p-ZAP7(Y319) and total ZAP70. Densitometry was performed on immunoblots across three biological replicates. Shown are mean ± SD. Primary murine CD4 + T cells were activated under Th17 (TCR+TGF-β+IL-6) or Treg polarization conditions (TCR+TGF-β) for 10 min in the presence or absence of 200 nM JAK2 inhibitor. B , immunoblotting was performed for p-ZAP7(Y319), ZAP70, p-CSK-S364, and CSK. Densitometry was performed on immunoblots across three biological replicates from panel B to determine the relative amount of ( C ) p-CSK-S364 and ( D ) p-ZAP70(Y319) normalized to total CSK and Zap70 abundance respectively. Shown are mean ± SD; p values were calculated by one-way ANOVA. E , primary murine CD4 + T cells were activated under Th17 (TCR+ TGF-β+IL-6) or Treg polarization conditions (TCR+ TGF-β) for 10 min in the presence or absence of 200 nM JAK2 inhibitor. Immunoblotting was performed for p-P85 (Y458) and P85. F , densitometry was performed on immunoblots across three biological replicates from panel E were p-P85(Y458) was normalized to total P85. Shown are mean ± SD; p values were calculated by one-way ANOVA. Mass ELISA assays were utilized to determine the relative level of ( G ) PtdIns(3,4,5)P3, and ( H ) <t>PtdIns(4,5)P2</t> generated in primary murine CD4 + T cells activated under Th17 or Treg polarization conditions for 10 min in the presence or absence of the JAK2 inhibitor. Shown are mean ± SD from three biological replicates; p values were calculated by one-way ANOVA. I , primary murine CD4 + T cells were activated for 10 min with constant amounts of anti-CD3 antibody, anti-CD28 antibody, and TGF-β with varying amounts of IL-6. Immunoblotting was performed for p-AKT(S473) and total AKT. Densitometry was performed on immunoblots across three biological replicates. Shown are mean ± SD. Source data are provided for the immunoblots in panels A , B , E , and I .
    Biotinylated Anti Ptdins 4 5 P2 Igm, supplied by Echelon Biosciences, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
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    93
    Echelon Biosciences ptdins
    JAK2 inhibition dysregulates signaling networks during Th17 polarization. A , primary murine CD4 + T cells were activated for 10 min with constant amounts of anti-CD3 antibody, soluble anti-CD28 antibody, and TGF-β with varying amounts of IL-6. Immunoblotting was performed for p-ZAP7(Y319) and total ZAP70. Densitometry was performed on immunoblots across three biological replicates. Shown are mean ± SD. Primary murine CD4 + T cells were activated under Th17 (TCR+TGF-β+IL-6) or Treg polarization conditions (TCR+TGF-β) for 10 min in the presence or absence of 200 nM JAK2 inhibitor. B , immunoblotting was performed for p-ZAP7(Y319), ZAP70, p-CSK-S364, and CSK. Densitometry was performed on immunoblots across three biological replicates from panel B to determine the relative amount of ( C ) p-CSK-S364 and ( D ) p-ZAP70(Y319) normalized to total CSK and Zap70 abundance respectively. Shown are mean ± SD; p values were calculated by one-way ANOVA. E , primary murine CD4 + T cells were activated under Th17 (TCR+ TGF-β+IL-6) or Treg polarization conditions (TCR+ TGF-β) for 10 min in the presence or absence of 200 nM JAK2 inhibitor. Immunoblotting was performed for p-P85 (Y458) and P85. F , densitometry was performed on immunoblots across three biological replicates from panel E were p-P85(Y458) was normalized to total P85. Shown are mean ± SD; p values were calculated by one-way ANOVA. Mass ELISA assays were utilized to determine the relative level of ( G ) <t>PtdIns(3,4,5)P3,</t> and ( H ) PtdIns(4,5)P2 generated in primary murine CD4 + T cells activated under Th17 or Treg polarization conditions for 10 min in the presence or absence of the JAK2 inhibitor. Shown are mean ± SD from three biological replicates; p values were calculated by one-way ANOVA. I , primary murine CD4 + T cells were activated for 10 min with constant amounts of anti-CD3 antibody, anti-CD28 antibody, and TGF-β with varying amounts of IL-6. Immunoblotting was performed for p-AKT(S473) and total AKT. Densitometry was performed on immunoblots across three biological replicates. Shown are mean ± SD. Source data are provided for the immunoblots in panels A , B , E , and I .
    Ptdins, supplied by Echelon Biosciences, 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/ptdins/product/Echelon Biosciences
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    ptdins - by Bioz Stars, 2022-09
    93/100 stars
      Buy from Supplier

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    JAK2 inhibition dysregulates signaling networks during Th17 polarization. A , primary murine CD4 + T cells were activated for 10 min with constant amounts of anti-CD3 antibody, soluble anti-CD28 antibody, and TGF-β with varying amounts of IL-6. Immunoblotting was performed for p-ZAP7(Y319) and total ZAP70. Densitometry was performed on immunoblots across three biological replicates. Shown are mean ± SD. Primary murine CD4 + T cells were activated under Th17 (TCR+TGF-β+IL-6) or Treg polarization conditions (TCR+TGF-β) for 10 min in the presence or absence of 200 nM JAK2 inhibitor. B , immunoblotting was performed for p-ZAP7(Y319), ZAP70, p-CSK-S364, and CSK. Densitometry was performed on immunoblots across three biological replicates from panel B to determine the relative amount of ( C ) p-CSK-S364 and ( D ) p-ZAP70(Y319) normalized to total CSK and Zap70 abundance respectively. Shown are mean ± SD; p values were calculated by one-way ANOVA. E , primary murine CD4 + T cells were activated under Th17 (TCR+ TGF-β+IL-6) or Treg polarization conditions (TCR+ TGF-β) for 10 min in the presence or absence of 200 nM JAK2 inhibitor. Immunoblotting was performed for p-P85 (Y458) and P85. F , densitometry was performed on immunoblots across three biological replicates from panel E were p-P85(Y458) was normalized to total P85. Shown are mean ± SD; p values were calculated by one-way ANOVA. Mass ELISA assays were utilized to determine the relative level of ( G ) PtdIns(3,4,5)P3, and ( H ) PtdIns(4,5)P2 generated in primary murine CD4 + T cells activated under Th17 or Treg polarization conditions for 10 min in the presence or absence of the JAK2 inhibitor. Shown are mean ± SD from three biological replicates; p values were calculated by one-way ANOVA. I , primary murine CD4 + T cells were activated for 10 min with constant amounts of anti-CD3 antibody, anti-CD28 antibody, and TGF-β with varying amounts of IL-6. Immunoblotting was performed for p-AKT(S473) and total AKT. Densitometry was performed on immunoblots across three biological replicates. Shown are mean ± SD. Source data are provided for the immunoblots in panels A , B , E , and I .

    Journal: The Journal of Biological Chemistry

    Article Title: Synergistic and additive interactions between receptor signaling networks drive the regulatory T cell versus T helper 17 cell fate choice

    doi: 10.1016/j.jbc.2021.101330

    Figure Lengend Snippet: JAK2 inhibition dysregulates signaling networks during Th17 polarization. A , primary murine CD4 + T cells were activated for 10 min with constant amounts of anti-CD3 antibody, soluble anti-CD28 antibody, and TGF-β with varying amounts of IL-6. Immunoblotting was performed for p-ZAP7(Y319) and total ZAP70. Densitometry was performed on immunoblots across three biological replicates. Shown are mean ± SD. Primary murine CD4 + T cells were activated under Th17 (TCR+TGF-β+IL-6) or Treg polarization conditions (TCR+TGF-β) for 10 min in the presence or absence of 200 nM JAK2 inhibitor. B , immunoblotting was performed for p-ZAP7(Y319), ZAP70, p-CSK-S364, and CSK. Densitometry was performed on immunoblots across three biological replicates from panel B to determine the relative amount of ( C ) p-CSK-S364 and ( D ) p-ZAP70(Y319) normalized to total CSK and Zap70 abundance respectively. Shown are mean ± SD; p values were calculated by one-way ANOVA. E , primary murine CD4 + T cells were activated under Th17 (TCR+ TGF-β+IL-6) or Treg polarization conditions (TCR+ TGF-β) for 10 min in the presence or absence of 200 nM JAK2 inhibitor. Immunoblotting was performed for p-P85 (Y458) and P85. F , densitometry was performed on immunoblots across three biological replicates from panel E were p-P85(Y458) was normalized to total P85. Shown are mean ± SD; p values were calculated by one-way ANOVA. Mass ELISA assays were utilized to determine the relative level of ( G ) PtdIns(3,4,5)P3, and ( H ) PtdIns(4,5)P2 generated in primary murine CD4 + T cells activated under Th17 or Treg polarization conditions for 10 min in the presence or absence of the JAK2 inhibitor. Shown are mean ± SD from three biological replicates; p values were calculated by one-way ANOVA. I , primary murine CD4 + T cells were activated for 10 min with constant amounts of anti-CD3 antibody, anti-CD28 antibody, and TGF-β with varying amounts of IL-6. Immunoblotting was performed for p-AKT(S473) and total AKT. Densitometry was performed on immunoblots across three biological replicates. Shown are mean ± SD. Source data are provided for the immunoblots in panels A , B , E , and I .

    Article Snippet: Cells were also stained with antibodies against PtdIns(4,5)-PE (Echelon Biosciences Z-B045) or PtdIns(3,4,5)P3-PE (Echelon Biosciences Z-B3345B).

    Techniques: Inhibition, Western Blot, Enzyme-linked Immunosorbent Assay, Generated

    JAK2 inhibition dysregulates signaling networks during Th17 polarization. A , primary murine CD4 + T cells were activated for 10 min with constant amounts of anti-CD3 antibody, soluble anti-CD28 antibody, and TGF-β with varying amounts of IL-6. Immunoblotting was performed for p-ZAP7(Y319) and total ZAP70. Densitometry was performed on immunoblots across three biological replicates. Shown are mean ± SD. Primary murine CD4 + T cells were activated under Th17 (TCR+TGF-β+IL-6) or Treg polarization conditions (TCR+TGF-β) for 10 min in the presence or absence of 200 nM JAK2 inhibitor. B , immunoblotting was performed for p-ZAP7(Y319), ZAP70, p-CSK-S364, and CSK. Densitometry was performed on immunoblots across three biological replicates from panel B to determine the relative amount of ( C ) p-CSK-S364 and ( D ) p-ZAP70(Y319) normalized to total CSK and Zap70 abundance respectively. Shown are mean ± SD; p values were calculated by one-way ANOVA. E , primary murine CD4 + T cells were activated under Th17 (TCR+ TGF-β+IL-6) or Treg polarization conditions (TCR+ TGF-β) for 10 min in the presence or absence of 200 nM JAK2 inhibitor. Immunoblotting was performed for p-P85 (Y458) and P85. F , densitometry was performed on immunoblots across three biological replicates from panel E were p-P85(Y458) was normalized to total P85. Shown are mean ± SD; p values were calculated by one-way ANOVA. Mass ELISA assays were utilized to determine the relative level of ( G ) PtdIns(3,4,5)P3, and ( H ) PtdIns(4,5)P2 generated in primary murine CD4 + T cells activated under Th17 or Treg polarization conditions for 10 min in the presence or absence of the JAK2 inhibitor. Shown are mean ± SD from three biological replicates; p values were calculated by one-way ANOVA. I , primary murine CD4 + T cells were activated for 10 min with constant amounts of anti-CD3 antibody, anti-CD28 antibody, and TGF-β with varying amounts of IL-6. Immunoblotting was performed for p-AKT(S473) and total AKT. Densitometry was performed on immunoblots across three biological replicates. Shown are mean ± SD. Source data are provided for the immunoblots in panels A , B , E , and I .

    Journal: The Journal of Biological Chemistry

    Article Title: Synergistic and additive interactions between receptor signaling networks drive the regulatory T cell versus T helper 17 cell fate choice

    doi: 10.1016/j.jbc.2021.101330

    Figure Lengend Snippet: JAK2 inhibition dysregulates signaling networks during Th17 polarization. A , primary murine CD4 + T cells were activated for 10 min with constant amounts of anti-CD3 antibody, soluble anti-CD28 antibody, and TGF-β with varying amounts of IL-6. Immunoblotting was performed for p-ZAP7(Y319) and total ZAP70. Densitometry was performed on immunoblots across three biological replicates. Shown are mean ± SD. Primary murine CD4 + T cells were activated under Th17 (TCR+TGF-β+IL-6) or Treg polarization conditions (TCR+TGF-β) for 10 min in the presence or absence of 200 nM JAK2 inhibitor. B , immunoblotting was performed for p-ZAP7(Y319), ZAP70, p-CSK-S364, and CSK. Densitometry was performed on immunoblots across three biological replicates from panel B to determine the relative amount of ( C ) p-CSK-S364 and ( D ) p-ZAP70(Y319) normalized to total CSK and Zap70 abundance respectively. Shown are mean ± SD; p values were calculated by one-way ANOVA. E , primary murine CD4 + T cells were activated under Th17 (TCR+ TGF-β+IL-6) or Treg polarization conditions (TCR+ TGF-β) for 10 min in the presence or absence of 200 nM JAK2 inhibitor. Immunoblotting was performed for p-P85 (Y458) and P85. F , densitometry was performed on immunoblots across three biological replicates from panel E were p-P85(Y458) was normalized to total P85. Shown are mean ± SD; p values were calculated by one-way ANOVA. Mass ELISA assays were utilized to determine the relative level of ( G ) PtdIns(3,4,5)P3, and ( H ) PtdIns(4,5)P2 generated in primary murine CD4 + T cells activated under Th17 or Treg polarization conditions for 10 min in the presence or absence of the JAK2 inhibitor. Shown are mean ± SD from three biological replicates; p values were calculated by one-way ANOVA. I , primary murine CD4 + T cells were activated for 10 min with constant amounts of anti-CD3 antibody, anti-CD28 antibody, and TGF-β with varying amounts of IL-6. Immunoblotting was performed for p-AKT(S473) and total AKT. Densitometry was performed on immunoblots across three biological replicates. Shown are mean ± SD. Source data are provided for the immunoblots in panels A , B , E , and I .

    Article Snippet: Cells were also stained with antibodies against PtdIns(4,5)-PE (Echelon Biosciences Z-B045) or PtdIns(3,4,5)P3-PE (Echelon Biosciences Z-B3345B).

    Techniques: Inhibition, Western Blot, Enzyme-linked Immunosorbent Assay, Generated