Review



rabbit anti stat1 py701  (Cell Signaling Technology Inc)


Bioz Verified Symbol Cell Signaling Technology Inc is a verified supplier
Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 98
      Buy from Supplier

    Structured Review

    Cell Signaling Technology Inc rabbit anti stat1 py701
    Fig. 4. Phosphorylation of PLEKHG3 at S1081 can be mediated by an IFN-regulated kinase in vitro and is required for interaction with 14-3-3 proteins. (A) Phosphopeptide intensities of the PLEKHG3 pS1081 phosphopeptide after stimulation with IFNα2, IFNβ, or IFNω for 90 min from the original LC-MS/MS data. Results from the five independent experiments in the screen are shown, and bars represent mean values with SD. Significance was determined by one-way ANOVA (*P ≤ 0.05). (B) Depiction of a consensus 14-3-3 binding motif and the corresponding sequence in PLEKHG3 surrounding the phosphorylation site at S1081. pS represents phosphorylated serine, and X represents any amino acid. (C and D) HEK293T cells were transiently transfected with 3xFlag-PLEKHG3 WT or the S1081A mutant. PLEKHG3 was then immunoprecipitated from lysates using an antibody against the Flag tag. Immunocomplexes were treated with λ-phosphatase where indicated, and subjected to an in vitro KA with recombinant Flag-IKKε (D). Immunoprecipitates (IP) and total lysates (TL) were analyzed by western blotting with the indicated antibodies. Data shown are representative of at least n = 3 independent experiments. (E–G) HEK293T cells were transiently transfected with 3xFlag-PLEKHG3 WT or the S1081A mutant, together with HA-tagged 14-3-3 proteins or GFP as indicated. 14-3-3 proteins or GFP were immunoprecipitated from lysates using an antibody against the HA-tag. IP and TL were analyzed by western blotting with the indicated antibodies. PLEKHG3 band intensities in IP in (E) were quantified using Image Studio Lite and are shown in (F), where bars represent mean values and SD from n = 3 independent experiments (each dot corresponds to one replicate). Significance compared with 14-3-3β was determined by the one-sample t test on log-transformed data (only significant comparisons are shown: *P ≤ 0.05; **P ≤ 0.01). (H and I) A549 cells were transfected with negative-control siRNAs, an siRNA targeting IRF9, or siRNA pools targeting all seven 14-3-3 family members (14-3-3β, 14-3-3γ, 14-3-3ε, 14-3-3ζ, 14-3-3η, 14-3-3θ, 14-3-3σ). 48 h post transfection, cells were stimulated with IFNα2 (1 ng/mL) for 4 h. Cells were harvested and IFIT2 mRNA levels were determined by RT-qPCR (H). Parallel cells were infected with VSV-GFP (MOI = 1 PFU/cell) and GFP expression as a measure for viral replication was assessed at 24 hpi (I). Bars represent mean values and SD from n = 3 independent experiments (each dot corresponds to one replicate). Significance was determined by two-way ANOVA with Dunnett’s multiple comparison test on log-transformed data (**P ≤ 0.01; ***P ≤ 0.001; ns, nonsignificant). (J) Schematic model for the hypothetical role of the PLEKHG3:14-3-3 axis in IFN signaling: We suggest that IFN-activated IKKε phosphorylates PLEKHG3 and facilitates the interaction of PLEKHG3 with one or more 14-3-3 proteins to regulate signal transduction downstream of <t>STAT1/STAT2</t> phosphorylation.
    Rabbit Anti Stat1 Py701, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1536 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti stat1 py701/product/Cell Signaling Technology Inc
    Average 98 stars, based on 1536 article reviews
    rabbit anti stat1 py701 - by Bioz Stars, 2026-03
    98/100 stars

    Images

    1) Product Images from "An atlas of protein phosphorylation dynamics during interferon signaling."

    Article Title: An atlas of protein phosphorylation dynamics during interferon signaling.

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    doi: 10.1073/pnas.2412990122

    Fig. 4. Phosphorylation of PLEKHG3 at S1081 can be mediated by an IFN-regulated kinase in vitro and is required for interaction with 14-3-3 proteins. (A) Phosphopeptide intensities of the PLEKHG3 pS1081 phosphopeptide after stimulation with IFNα2, IFNβ, or IFNω for 90 min from the original LC-MS/MS data. Results from the five independent experiments in the screen are shown, and bars represent mean values with SD. Significance was determined by one-way ANOVA (*P ≤ 0.05). (B) Depiction of a consensus 14-3-3 binding motif and the corresponding sequence in PLEKHG3 surrounding the phosphorylation site at S1081. pS represents phosphorylated serine, and X represents any amino acid. (C and D) HEK293T cells were transiently transfected with 3xFlag-PLEKHG3 WT or the S1081A mutant. PLEKHG3 was then immunoprecipitated from lysates using an antibody against the Flag tag. Immunocomplexes were treated with λ-phosphatase where indicated, and subjected to an in vitro KA with recombinant Flag-IKKε (D). Immunoprecipitates (IP) and total lysates (TL) were analyzed by western blotting with the indicated antibodies. Data shown are representative of at least n = 3 independent experiments. (E–G) HEK293T cells were transiently transfected with 3xFlag-PLEKHG3 WT or the S1081A mutant, together with HA-tagged 14-3-3 proteins or GFP as indicated. 14-3-3 proteins or GFP were immunoprecipitated from lysates using an antibody against the HA-tag. IP and TL were analyzed by western blotting with the indicated antibodies. PLEKHG3 band intensities in IP in (E) were quantified using Image Studio Lite and are shown in (F), where bars represent mean values and SD from n = 3 independent experiments (each dot corresponds to one replicate). Significance compared with 14-3-3β was determined by the one-sample t test on log-transformed data (only significant comparisons are shown: *P ≤ 0.05; **P ≤ 0.01). (H and I) A549 cells were transfected with negative-control siRNAs, an siRNA targeting IRF9, or siRNA pools targeting all seven 14-3-3 family members (14-3-3β, 14-3-3γ, 14-3-3ε, 14-3-3ζ, 14-3-3η, 14-3-3θ, 14-3-3σ). 48 h post transfection, cells were stimulated with IFNα2 (1 ng/mL) for 4 h. Cells were harvested and IFIT2 mRNA levels were determined by RT-qPCR (H). Parallel cells were infected with VSV-GFP (MOI = 1 PFU/cell) and GFP expression as a measure for viral replication was assessed at 24 hpi (I). Bars represent mean values and SD from n = 3 independent experiments (each dot corresponds to one replicate). Significance was determined by two-way ANOVA with Dunnett’s multiple comparison test on log-transformed data (**P ≤ 0.01; ***P ≤ 0.001; ns, nonsignificant). (J) Schematic model for the hypothetical role of the PLEKHG3:14-3-3 axis in IFN signaling: We suggest that IFN-activated IKKε phosphorylates PLEKHG3 and facilitates the interaction of PLEKHG3 with one or more 14-3-3 proteins to regulate signal transduction downstream of STAT1/STAT2 phosphorylation.
    Figure Legend Snippet: Fig. 4. Phosphorylation of PLEKHG3 at S1081 can be mediated by an IFN-regulated kinase in vitro and is required for interaction with 14-3-3 proteins. (A) Phosphopeptide intensities of the PLEKHG3 pS1081 phosphopeptide after stimulation with IFNα2, IFNβ, or IFNω for 90 min from the original LC-MS/MS data. Results from the five independent experiments in the screen are shown, and bars represent mean values with SD. Significance was determined by one-way ANOVA (*P ≤ 0.05). (B) Depiction of a consensus 14-3-3 binding motif and the corresponding sequence in PLEKHG3 surrounding the phosphorylation site at S1081. pS represents phosphorylated serine, and X represents any amino acid. (C and D) HEK293T cells were transiently transfected with 3xFlag-PLEKHG3 WT or the S1081A mutant. PLEKHG3 was then immunoprecipitated from lysates using an antibody against the Flag tag. Immunocomplexes were treated with λ-phosphatase where indicated, and subjected to an in vitro KA with recombinant Flag-IKKε (D). Immunoprecipitates (IP) and total lysates (TL) were analyzed by western blotting with the indicated antibodies. Data shown are representative of at least n = 3 independent experiments. (E–G) HEK293T cells were transiently transfected with 3xFlag-PLEKHG3 WT or the S1081A mutant, together with HA-tagged 14-3-3 proteins or GFP as indicated. 14-3-3 proteins or GFP were immunoprecipitated from lysates using an antibody against the HA-tag. IP and TL were analyzed by western blotting with the indicated antibodies. PLEKHG3 band intensities in IP in (E) were quantified using Image Studio Lite and are shown in (F), where bars represent mean values and SD from n = 3 independent experiments (each dot corresponds to one replicate). Significance compared with 14-3-3β was determined by the one-sample t test on log-transformed data (only significant comparisons are shown: *P ≤ 0.05; **P ≤ 0.01). (H and I) A549 cells were transfected with negative-control siRNAs, an siRNA targeting IRF9, or siRNA pools targeting all seven 14-3-3 family members (14-3-3β, 14-3-3γ, 14-3-3ε, 14-3-3ζ, 14-3-3η, 14-3-3θ, 14-3-3σ). 48 h post transfection, cells were stimulated with IFNα2 (1 ng/mL) for 4 h. Cells were harvested and IFIT2 mRNA levels were determined by RT-qPCR (H). Parallel cells were infected with VSV-GFP (MOI = 1 PFU/cell) and GFP expression as a measure for viral replication was assessed at 24 hpi (I). Bars represent mean values and SD from n = 3 independent experiments (each dot corresponds to one replicate). Significance was determined by two-way ANOVA with Dunnett’s multiple comparison test on log-transformed data (**P ≤ 0.01; ***P ≤ 0.001; ns, nonsignificant). (J) Schematic model for the hypothetical role of the PLEKHG3:14-3-3 axis in IFN signaling: We suggest that IFN-activated IKKε phosphorylates PLEKHG3 and facilitates the interaction of PLEKHG3 with one or more 14-3-3 proteins to regulate signal transduction downstream of STAT1/STAT2 phosphorylation.

    Techniques Used: Phospho-proteomics, In Vitro, Liquid Chromatography with Mass Spectroscopy, Binding Assay, Sequencing, Transfection, Mutagenesis, Immunoprecipitation, FLAG-tag, Recombinant, Western Blot, Transformation Assay, Negative Control, Quantitative RT-PCR, Infection, Expressing, Comparison, Transduction



    Similar Products

    rabbit anti stat1 py701  (Cell Signaling Technology Inc)
    98
    Cell Signaling Technology Inc rabbit anti stat1 py701
    Fig. 4. Phosphorylation of PLEKHG3 at S1081 can be mediated by an IFN-regulated kinase in vitro and is required for interaction with 14-3-3 proteins. (A) Phosphopeptide intensities of the PLEKHG3 pS1081 phosphopeptide after stimulation with IFNα2, IFNβ, or IFNω for 90 min from the original LC-MS/MS data. Results from the five independent experiments in the screen are shown, and bars represent mean values with SD. Significance was determined by one-way ANOVA (*P ≤ 0.05). (B) Depiction of a consensus 14-3-3 binding motif and the corresponding sequence in PLEKHG3 surrounding the phosphorylation site at S1081. pS represents phosphorylated serine, and X represents any amino acid. (C and D) HEK293T cells were transiently transfected with 3xFlag-PLEKHG3 WT or the S1081A mutant. PLEKHG3 was then immunoprecipitated from lysates using an antibody against the Flag tag. Immunocomplexes were treated with λ-phosphatase where indicated, and subjected to an in vitro KA with recombinant Flag-IKKε (D). Immunoprecipitates (IP) and total lysates (TL) were analyzed by western blotting with the indicated antibodies. Data shown are representative of at least n = 3 independent experiments. (E–G) HEK293T cells were transiently transfected with 3xFlag-PLEKHG3 WT or the S1081A mutant, together with HA-tagged 14-3-3 proteins or GFP as indicated. 14-3-3 proteins or GFP were immunoprecipitated from lysates using an antibody against the HA-tag. IP and TL were analyzed by western blotting with the indicated antibodies. PLEKHG3 band intensities in IP in (E) were quantified using Image Studio Lite and are shown in (F), where bars represent mean values and SD from n = 3 independent experiments (each dot corresponds to one replicate). Significance compared with 14-3-3β was determined by the one-sample t test on log-transformed data (only significant comparisons are shown: *P ≤ 0.05; **P ≤ 0.01). (H and I) A549 cells were transfected with negative-control siRNAs, an siRNA targeting IRF9, or siRNA pools targeting all seven 14-3-3 family members (14-3-3β, 14-3-3γ, 14-3-3ε, 14-3-3ζ, 14-3-3η, 14-3-3θ, 14-3-3σ). 48 h post transfection, cells were stimulated with IFNα2 (1 ng/mL) for 4 h. Cells were harvested and IFIT2 mRNA levels were determined by RT-qPCR (H). Parallel cells were infected with VSV-GFP (MOI = 1 PFU/cell) and GFP expression as a measure for viral replication was assessed at 24 hpi (I). Bars represent mean values and SD from n = 3 independent experiments (each dot corresponds to one replicate). Significance was determined by two-way ANOVA with Dunnett’s multiple comparison test on log-transformed data (**P ≤ 0.01; ***P ≤ 0.001; ns, nonsignificant). (J) Schematic model for the hypothetical role of the PLEKHG3:14-3-3 axis in IFN signaling: We suggest that IFN-activated IKKε phosphorylates PLEKHG3 and facilitates the interaction of PLEKHG3 with one or more 14-3-3 proteins to regulate signal transduction downstream of <t>STAT1/STAT2</t> phosphorylation.
    Rabbit Anti Stat1 Py701, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti stat1 py701/product/Cell Signaling Technology Inc
    Average 98 stars, based on 1 article reviews
    rabbit anti stat1 py701 - by Bioz Stars, 2026-03
    98/100 stars
    		  Buy from Supplier
    stat1 py701  (Cell Signaling Technology Inc)
    98
    Cell Signaling Technology Inc stat1 py701
    Fig. 4. Phosphorylation of PLEKHG3 at S1081 can be mediated by an IFN-regulated kinase in vitro and is required for interaction with 14-3-3 proteins. (A) Phosphopeptide intensities of the PLEKHG3 pS1081 phosphopeptide after stimulation with IFNα2, IFNβ, or IFNω for 90 min from the original LC-MS/MS data. Results from the five independent experiments in the screen are shown, and bars represent mean values with SD. Significance was determined by one-way ANOVA (*P ≤ 0.05). (B) Depiction of a consensus 14-3-3 binding motif and the corresponding sequence in PLEKHG3 surrounding the phosphorylation site at S1081. pS represents phosphorylated serine, and X represents any amino acid. (C and D) HEK293T cells were transiently transfected with 3xFlag-PLEKHG3 WT or the S1081A mutant. PLEKHG3 was then immunoprecipitated from lysates using an antibody against the Flag tag. Immunocomplexes were treated with λ-phosphatase where indicated, and subjected to an in vitro KA with recombinant Flag-IKKε (D). Immunoprecipitates (IP) and total lysates (TL) were analyzed by western blotting with the indicated antibodies. Data shown are representative of at least n = 3 independent experiments. (E–G) HEK293T cells were transiently transfected with 3xFlag-PLEKHG3 WT or the S1081A mutant, together with HA-tagged 14-3-3 proteins or GFP as indicated. 14-3-3 proteins or GFP were immunoprecipitated from lysates using an antibody against the HA-tag. IP and TL were analyzed by western blotting with the indicated antibodies. PLEKHG3 band intensities in IP in (E) were quantified using Image Studio Lite and are shown in (F), where bars represent mean values and SD from n = 3 independent experiments (each dot corresponds to one replicate). Significance compared with 14-3-3β was determined by the one-sample t test on log-transformed data (only significant comparisons are shown: *P ≤ 0.05; **P ≤ 0.01). (H and I) A549 cells were transfected with negative-control siRNAs, an siRNA targeting IRF9, or siRNA pools targeting all seven 14-3-3 family members (14-3-3β, 14-3-3γ, 14-3-3ε, 14-3-3ζ, 14-3-3η, 14-3-3θ, 14-3-3σ). 48 h post transfection, cells were stimulated with IFNα2 (1 ng/mL) for 4 h. Cells were harvested and IFIT2 mRNA levels were determined by RT-qPCR (H). Parallel cells were infected with VSV-GFP (MOI = 1 PFU/cell) and GFP expression as a measure for viral replication was assessed at 24 hpi (I). Bars represent mean values and SD from n = 3 independent experiments (each dot corresponds to one replicate). Significance was determined by two-way ANOVA with Dunnett’s multiple comparison test on log-transformed data (**P ≤ 0.01; ***P ≤ 0.001; ns, nonsignificant). (J) Schematic model for the hypothetical role of the PLEKHG3:14-3-3 axis in IFN signaling: We suggest that IFN-activated IKKε phosphorylates PLEKHG3 and facilitates the interaction of PLEKHG3 with one or more 14-3-3 proteins to regulate signal transduction downstream of <t>STAT1/STAT2</t> phosphorylation.
    Stat1 Py701, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/stat1 py701/product/Cell Signaling Technology Inc
    Average 98 stars, based on 1 article reviews
    stat1 py701 - by Bioz Stars, 2026-03
    98/100 stars
    		  Buy from Supplier
    phospho stat1 py701  (Cell Signaling Technology Inc)
    96
    Cell Signaling Technology Inc phospho stat1 py701
    Fig. 4. Phosphorylation of PLEKHG3 at S1081 can be mediated by an IFN-regulated kinase in vitro and is required for interaction with 14-3-3 proteins. (A) Phosphopeptide intensities of the PLEKHG3 pS1081 phosphopeptide after stimulation with IFNα2, IFNβ, or IFNω for 90 min from the original LC-MS/MS data. Results from the five independent experiments in the screen are shown, and bars represent mean values with SD. Significance was determined by one-way ANOVA (*P ≤ 0.05). (B) Depiction of a consensus 14-3-3 binding motif and the corresponding sequence in PLEKHG3 surrounding the phosphorylation site at S1081. pS represents phosphorylated serine, and X represents any amino acid. (C and D) HEK293T cells were transiently transfected with 3xFlag-PLEKHG3 WT or the S1081A mutant. PLEKHG3 was then immunoprecipitated from lysates using an antibody against the Flag tag. Immunocomplexes were treated with λ-phosphatase where indicated, and subjected to an in vitro KA with recombinant Flag-IKKε (D). Immunoprecipitates (IP) and total lysates (TL) were analyzed by western blotting with the indicated antibodies. Data shown are representative of at least n = 3 independent experiments. (E–G) HEK293T cells were transiently transfected with 3xFlag-PLEKHG3 WT or the S1081A mutant, together with HA-tagged 14-3-3 proteins or GFP as indicated. 14-3-3 proteins or GFP were immunoprecipitated from lysates using an antibody against the HA-tag. IP and TL were analyzed by western blotting with the indicated antibodies. PLEKHG3 band intensities in IP in (E) were quantified using Image Studio Lite and are shown in (F), where bars represent mean values and SD from n = 3 independent experiments (each dot corresponds to one replicate). Significance compared with 14-3-3β was determined by the one-sample t test on log-transformed data (only significant comparisons are shown: *P ≤ 0.05; **P ≤ 0.01). (H and I) A549 cells were transfected with negative-control siRNAs, an siRNA targeting IRF9, or siRNA pools targeting all seven 14-3-3 family members (14-3-3β, 14-3-3γ, 14-3-3ε, 14-3-3ζ, 14-3-3η, 14-3-3θ, 14-3-3σ). 48 h post transfection, cells were stimulated with IFNα2 (1 ng/mL) for 4 h. Cells were harvested and IFIT2 mRNA levels were determined by RT-qPCR (H). Parallel cells were infected with VSV-GFP (MOI = 1 PFU/cell) and GFP expression as a measure for viral replication was assessed at 24 hpi (I). Bars represent mean values and SD from n = 3 independent experiments (each dot corresponds to one replicate). Significance was determined by two-way ANOVA with Dunnett’s multiple comparison test on log-transformed data (**P ≤ 0.01; ***P ≤ 0.001; ns, nonsignificant). (J) Schematic model for the hypothetical role of the PLEKHG3:14-3-3 axis in IFN signaling: We suggest that IFN-activated IKKε phosphorylates PLEKHG3 and facilitates the interaction of PLEKHG3 with one or more 14-3-3 proteins to regulate signal transduction downstream of <t>STAT1/STAT2</t> phosphorylation.
    Phospho Stat1 Py701, supplied by Cell Signaling Technology Inc, 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/phospho stat1 py701/product/Cell Signaling Technology Inc
    Average 96 stars, based on 1 article reviews
    phospho stat1 py701 - by Bioz Stars, 2026-03
    96/100 stars
    		  Buy from Supplier
    anti human phospho stat1 py701 monoclonal antibody  (Cell Signaling Technology Inc)
    98
    Cell Signaling Technology Inc anti human phospho stat1 py701 monoclonal antibody
    Effective neutralization of IFN-γ signaling by anti-IFN-γ autoAbs. (A) The representative histograms of the inhibitory effects on the IFN-γ-induced PE <t>(phycoerythrin)-STAT1</t> phosphorylation in THP-1 cells treated with serum samples from autoAbs-positive AOSD patients (P1, P2, and P4), autoAbs-negative patients (P7, P9, and P10), or HC subjects (H2, H3, and H4). (B) Comparison of pSTAT1 intensity after inhibition with serum samples from three groups subjects. (C, D) IgG depletion of serum (10%) from autoAbs-positive AOSD patients (P1 and P2) were restored the IFN-γ-induced STAT1 phosphorylation on THP-1 cells. (E) The inhibitory effects on IFN-γ-induced STAT1 phosphorylation on THP-1 cells treated with serum samples from autoAbs-positive AOSD patients (P1-P4), autoAbs-negative patients (P7-P10), or HC subjects (H1-H4). (F) Comparison of phosphorylated STAT1 (pSTAT1) intensity after inhibition with serum from three groups subjects. Bars and error bars indicate the mean and standard error of mean, respectively. The p-values were determined by One-Way ANOVA test using Bonferroni correction. * p < 0.05, ** p < 0.01.
    Anti Human Phospho Stat1 Py701 Monoclonal Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti human phospho stat1 py701 monoclonal antibody/product/Cell Signaling Technology Inc
    Average 98 stars, based on 1 article reviews
    anti human phospho stat1 py701 monoclonal antibody - by Bioz Stars, 2026-03
    98/100 stars
    		  Buy from Supplier
    py701 stat1  (Cell Signaling Technology Inc)
    95
    Cell Signaling Technology Inc py701 stat1
    Effective neutralization of IFN-γ signaling by anti-IFN-γ autoAbs. (A) The representative histograms of the inhibitory effects on the IFN-γ-induced PE <t>(phycoerythrin)-STAT1</t> phosphorylation in THP-1 cells treated with serum samples from autoAbs-positive AOSD patients (P1, P2, and P4), autoAbs-negative patients (P7, P9, and P10), or HC subjects (H2, H3, and H4). (B) Comparison of pSTAT1 intensity after inhibition with serum samples from three groups subjects. (C, D) IgG depletion of serum (10%) from autoAbs-positive AOSD patients (P1 and P2) were restored the IFN-γ-induced STAT1 phosphorylation on THP-1 cells. (E) The inhibitory effects on IFN-γ-induced STAT1 phosphorylation on THP-1 cells treated with serum samples from autoAbs-positive AOSD patients (P1-P4), autoAbs-negative patients (P7-P10), or HC subjects (H1-H4). (F) Comparison of phosphorylated STAT1 (pSTAT1) intensity after inhibition with serum from three groups subjects. Bars and error bars indicate the mean and standard error of mean, respectively. The p-values were determined by One-Way ANOVA test using Bonferroni correction. * p < 0.05, ** p < 0.01.
    Py701 Stat1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/py701 stat1/product/Cell Signaling Technology Inc
    Average 95 stars, based on 1 article reviews
    py701 stat1 - by Bioz Stars, 2026-03
    95/100 stars
    		  Buy from Supplier
    antibodies rabbit anti py701 stat1  (Cell Signaling Technology Inc)
    96
    Cell Signaling Technology Inc antibodies rabbit anti py701 stat1
    Effective neutralization of IFN-γ signaling by anti-IFN-γ autoAbs. (A) The representative histograms of the inhibitory effects on the IFN-γ-induced PE <t>(phycoerythrin)-STAT1</t> phosphorylation in THP-1 cells treated with serum samples from autoAbs-positive AOSD patients (P1, P2, and P4), autoAbs-negative patients (P7, P9, and P10), or HC subjects (H2, H3, and H4). (B) Comparison of pSTAT1 intensity after inhibition with serum samples from three groups subjects. (C, D) IgG depletion of serum (10%) from autoAbs-positive AOSD patients (P1 and P2) were restored the IFN-γ-induced STAT1 phosphorylation on THP-1 cells. (E) The inhibitory effects on IFN-γ-induced STAT1 phosphorylation on THP-1 cells treated with serum samples from autoAbs-positive AOSD patients (P1-P4), autoAbs-negative patients (P7-P10), or HC subjects (H1-H4). (F) Comparison of phosphorylated STAT1 (pSTAT1) intensity after inhibition with serum from three groups subjects. Bars and error bars indicate the mean and standard error of mean, respectively. The p-values were determined by One-Way ANOVA test using Bonferroni correction. * p < 0.05, ** p < 0.01.
    Antibodies Rabbit Anti Py701 Stat1, supplied by Cell Signaling Technology Inc, 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/antibodies rabbit anti py701 stat1/product/Cell Signaling Technology Inc
    Average 96 stars, based on 1 article reviews
    antibodies rabbit anti py701 stat1 - by Bioz Stars, 2026-03
    96/100 stars
    		  Buy from Supplier
    antibodies rabbit anti py701 stat1  (Santa Cruz Biotechnology)
    94
    Santa Cruz Biotechnology antibodies rabbit anti py701 stat1
    Effective neutralization of IFN-γ signaling by anti-IFN-γ autoAbs. (A) The representative histograms of the inhibitory effects on the IFN-γ-induced PE <t>(phycoerythrin)-STAT1</t> phosphorylation in THP-1 cells treated with serum samples from autoAbs-positive AOSD patients (P1, P2, and P4), autoAbs-negative patients (P7, P9, and P10), or HC subjects (H2, H3, and H4). (B) Comparison of pSTAT1 intensity after inhibition with serum samples from three groups subjects. (C, D) IgG depletion of serum (10%) from autoAbs-positive AOSD patients (P1 and P2) were restored the IFN-γ-induced STAT1 phosphorylation on THP-1 cells. (E) The inhibitory effects on IFN-γ-induced STAT1 phosphorylation on THP-1 cells treated with serum samples from autoAbs-positive AOSD patients (P1-P4), autoAbs-negative patients (P7-P10), or HC subjects (H1-H4). (F) Comparison of phosphorylated STAT1 (pSTAT1) intensity after inhibition with serum from three groups subjects. Bars and error bars indicate the mean and standard error of mean, respectively. The p-values were determined by One-Way ANOVA test using Bonferroni correction. * p < 0.05, ** p < 0.01.
    Antibodies Rabbit Anti Py701 Stat1, supplied by Santa Cruz Biotechnology, 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/antibodies rabbit anti py701 stat1/product/Santa Cruz Biotechnology
    Average 94 stars, based on 1 article reviews
    antibodies rabbit anti py701 stat1 - by Bioz Stars, 2026-03
    94/100 stars
    		  Buy from Supplier

    Image Search Results


    Fig. 4. Phosphorylation of PLEKHG3 at S1081 can be mediated by an IFN-regulated kinase in vitro and is required for interaction with 14-3-3 proteins. (A) Phosphopeptide intensities of the PLEKHG3 pS1081 phosphopeptide after stimulation with IFNα2, IFNβ, or IFNω for 90 min from the original LC-MS/MS data. Results from the five independent experiments in the screen are shown, and bars represent mean values with SD. Significance was determined by one-way ANOVA (*P ≤ 0.05). (B) Depiction of a consensus 14-3-3 binding motif and the corresponding sequence in PLEKHG3 surrounding the phosphorylation site at S1081. pS represents phosphorylated serine, and X represents any amino acid. (C and D) HEK293T cells were transiently transfected with 3xFlag-PLEKHG3 WT or the S1081A mutant. PLEKHG3 was then immunoprecipitated from lysates using an antibody against the Flag tag. Immunocomplexes were treated with λ-phosphatase where indicated, and subjected to an in vitro KA with recombinant Flag-IKKε (D). Immunoprecipitates (IP) and total lysates (TL) were analyzed by western blotting with the indicated antibodies. Data shown are representative of at least n = 3 independent experiments. (E–G) HEK293T cells were transiently transfected with 3xFlag-PLEKHG3 WT or the S1081A mutant, together with HA-tagged 14-3-3 proteins or GFP as indicated. 14-3-3 proteins or GFP were immunoprecipitated from lysates using an antibody against the HA-tag. IP and TL were analyzed by western blotting with the indicated antibodies. PLEKHG3 band intensities in IP in (E) were quantified using Image Studio Lite and are shown in (F), where bars represent mean values and SD from n = 3 independent experiments (each dot corresponds to one replicate). Significance compared with 14-3-3β was determined by the one-sample t test on log-transformed data (only significant comparisons are shown: *P ≤ 0.05; **P ≤ 0.01). (H and I) A549 cells were transfected with negative-control siRNAs, an siRNA targeting IRF9, or siRNA pools targeting all seven 14-3-3 family members (14-3-3β, 14-3-3γ, 14-3-3ε, 14-3-3ζ, 14-3-3η, 14-3-3θ, 14-3-3σ). 48 h post transfection, cells were stimulated with IFNα2 (1 ng/mL) for 4 h. Cells were harvested and IFIT2 mRNA levels were determined by RT-qPCR (H). Parallel cells were infected with VSV-GFP (MOI = 1 PFU/cell) and GFP expression as a measure for viral replication was assessed at 24 hpi (I). Bars represent mean values and SD from n = 3 independent experiments (each dot corresponds to one replicate). Significance was determined by two-way ANOVA with Dunnett’s multiple comparison test on log-transformed data (**P ≤ 0.01; ***P ≤ 0.001; ns, nonsignificant). (J) Schematic model for the hypothetical role of the PLEKHG3:14-3-3 axis in IFN signaling: We suggest that IFN-activated IKKε phosphorylates PLEKHG3 and facilitates the interaction of PLEKHG3 with one or more 14-3-3 proteins to regulate signal transduction downstream of STAT1/STAT2 phosphorylation.

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    Article Title: An atlas of protein phosphorylation dynamics during interferon signaling.

    doi: 10.1073/pnas.2412990122

    Figure Lengend Snippet: Fig. 4. Phosphorylation of PLEKHG3 at S1081 can be mediated by an IFN-regulated kinase in vitro and is required for interaction with 14-3-3 proteins. (A) Phosphopeptide intensities of the PLEKHG3 pS1081 phosphopeptide after stimulation with IFNα2, IFNβ, or IFNω for 90 min from the original LC-MS/MS data. Results from the five independent experiments in the screen are shown, and bars represent mean values with SD. Significance was determined by one-way ANOVA (*P ≤ 0.05). (B) Depiction of a consensus 14-3-3 binding motif and the corresponding sequence in PLEKHG3 surrounding the phosphorylation site at S1081. pS represents phosphorylated serine, and X represents any amino acid. (C and D) HEK293T cells were transiently transfected with 3xFlag-PLEKHG3 WT or the S1081A mutant. PLEKHG3 was then immunoprecipitated from lysates using an antibody against the Flag tag. Immunocomplexes were treated with λ-phosphatase where indicated, and subjected to an in vitro KA with recombinant Flag-IKKε (D). Immunoprecipitates (IP) and total lysates (TL) were analyzed by western blotting with the indicated antibodies. Data shown are representative of at least n = 3 independent experiments. (E–G) HEK293T cells were transiently transfected with 3xFlag-PLEKHG3 WT or the S1081A mutant, together with HA-tagged 14-3-3 proteins or GFP as indicated. 14-3-3 proteins or GFP were immunoprecipitated from lysates using an antibody against the HA-tag. IP and TL were analyzed by western blotting with the indicated antibodies. PLEKHG3 band intensities in IP in (E) were quantified using Image Studio Lite and are shown in (F), where bars represent mean values and SD from n = 3 independent experiments (each dot corresponds to one replicate). Significance compared with 14-3-3β was determined by the one-sample t test on log-transformed data (only significant comparisons are shown: *P ≤ 0.05; **P ≤ 0.01). (H and I) A549 cells were transfected with negative-control siRNAs, an siRNA targeting IRF9, or siRNA pools targeting all seven 14-3-3 family members (14-3-3β, 14-3-3γ, 14-3-3ε, 14-3-3ζ, 14-3-3η, 14-3-3θ, 14-3-3σ). 48 h post transfection, cells were stimulated with IFNα2 (1 ng/mL) for 4 h. Cells were harvested and IFIT2 mRNA levels were determined by RT-qPCR (H). Parallel cells were infected with VSV-GFP (MOI = 1 PFU/cell) and GFP expression as a measure for viral replication was assessed at 24 hpi (I). Bars represent mean values and SD from n = 3 independent experiments (each dot corresponds to one replicate). Significance was determined by two-way ANOVA with Dunnett’s multiple comparison test on log-transformed data (**P ≤ 0.01; ***P ≤ 0.001; ns, nonsignificant). (J) Schematic model for the hypothetical role of the PLEKHG3:14-3-3 axis in IFN signaling: We suggest that IFN-activated IKKε phosphorylates PLEKHG3 and facilitates the interaction of PLEKHG3 with one or more 14-3-3 proteins to regulate signal transduction downstream of STAT1/STAT2 phosphorylation.

    Article Snippet: Primary antibodies used were rabbit anti- STAT1- pY701 (#9167, Cell Signaling); mouse anti- STAT1 (sc- 417, Santa Cruz); mouse anti- beta- actin (C4) (sc- 47778, Santa Cruz); mouse anti- ANXA2- pY24 (sc- 135753, Santa Cruz); mouse anti- ANXA2 (sc- 28385, Santa Cruz); rabbit anti- STAT1- pS727 (#9177, Cell Signaling); rabbit anti- STAT1 (#14994, Cell Signaling); mouse anti- MX1 (12), mouse anti- RIG- I (AG- 20B- 0009- C100, Adipogen); rabbit anti- IRF9 (#D2T8M, Cell Signaling); rabbit anti- STAT2- pY690 (#88410, Cell Signaling); mouse antiSTAT2 (A- 7) (sc- 1668, Santa Cruz); rabbit anti- Flag (F7425, Sigma Aldrich); mouse anti- Flag M2 (F1804, Sigma Aldrich); rabbit anti- pSer 14- 3- 3 Binding Motif (14- 3- 3 PBM) (#9601, Cell Signaling); rabbit anti- PLEKHG3 (PA5- 46053, Thermo Fisher Scientific); rabbit anti- HA (#3724, Cell Signaling); and mouse anti- HA (#2367, Cell Signaling).

    Techniques: Phospho-proteomics, In Vitro, Liquid Chromatography with Mass Spectroscopy, Binding Assay, Sequencing, Transfection, Mutagenesis, Immunoprecipitation, FLAG-tag, Recombinant, Western Blot, Transformation Assay, Negative Control, Quantitative RT-PCR, Infection, Expressing, Comparison, Transduction

    Effective neutralization of IFN-γ signaling by anti-IFN-γ autoAbs. (A) The representative histograms of the inhibitory effects on the IFN-γ-induced PE (phycoerythrin)-STAT1 phosphorylation in THP-1 cells treated with serum samples from autoAbs-positive AOSD patients (P1, P2, and P4), autoAbs-negative patients (P7, P9, and P10), or HC subjects (H2, H3, and H4). (B) Comparison of pSTAT1 intensity after inhibition with serum samples from three groups subjects. (C, D) IgG depletion of serum (10%) from autoAbs-positive AOSD patients (P1 and P2) were restored the IFN-γ-induced STAT1 phosphorylation on THP-1 cells. (E) The inhibitory effects on IFN-γ-induced STAT1 phosphorylation on THP-1 cells treated with serum samples from autoAbs-positive AOSD patients (P1-P4), autoAbs-negative patients (P7-P10), or HC subjects (H1-H4). (F) Comparison of phosphorylated STAT1 (pSTAT1) intensity after inhibition with serum from three groups subjects. Bars and error bars indicate the mean and standard error of mean, respectively. The p-values were determined by One-Way ANOVA test using Bonferroni correction. * p < 0.05, ** p < 0.01.

    Journal: Frontiers in Medicine

    Article Title: High-titer anti-interferon-γ neutralizing autoantibodies linked to opportunistic infections in patients with adult-onset still's disease

    doi: 10.3389/fmed.2022.1097514

    Figure Lengend Snippet: Effective neutralization of IFN-γ signaling by anti-IFN-γ autoAbs. (A) The representative histograms of the inhibitory effects on the IFN-γ-induced PE (phycoerythrin)-STAT1 phosphorylation in THP-1 cells treated with serum samples from autoAbs-positive AOSD patients (P1, P2, and P4), autoAbs-negative patients (P7, P9, and P10), or HC subjects (H2, H3, and H4). (B) Comparison of pSTAT1 intensity after inhibition with serum samples from three groups subjects. (C, D) IgG depletion of serum (10%) from autoAbs-positive AOSD patients (P1 and P2) were restored the IFN-γ-induced STAT1 phosphorylation on THP-1 cells. (E) The inhibitory effects on IFN-γ-induced STAT1 phosphorylation on THP-1 cells treated with serum samples from autoAbs-positive AOSD patients (P1-P4), autoAbs-negative patients (P7-P10), or HC subjects (H1-H4). (F) Comparison of phosphorylated STAT1 (pSTAT1) intensity after inhibition with serum from three groups subjects. Bars and error bars indicate the mean and standard error of mean, respectively. The p-values were determined by One-Way ANOVA test using Bonferroni correction. * p < 0.05, ** p < 0.01.

    Article Snippet: After blocking with 5% milk, immunoblots were performed by using specific anti-human phospho-STAT1 (pY701) monoclonal antibody (#9167), anti-human total-STAT-1 monoclonal antibody (#14994, Cell Signaling Technology, Danvers, MA, USA), and anti-human GAPDH antibody (Elabscience, Houston, TX, USA).

    Techniques: Neutralization, Phospho-proteomics, Comparison, Inhibition