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p stat1 y701  (Proteintech)


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    Structured Review

    Proteintech p stat1 y701
    HTATSF1 mediates viral nucleic acid- but not IFN-β-triggered signaling. (A) Effects of HTATSF1-deficiency on transcription of downstream genes induced by viral nucleic acid mimics. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were untransfected or transfected with HT-DNA (2 μg/mL) or poly(I:C) (2 μg/mL) for the indicated times before RT-qPCR analysis to measure mRNA levels of the indicated genes. (B) Effects of HTATSF1-deficiency on transcription of downstream genes induced by cGAMP. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were left untreated or treated with 2′3′-cGAMP (40 nM) for the indicated times before RT-qPCR analysis to measure mRNA levels of the indicated genes. (C) Effects of HTATSF1-deficiency on IFN-β-induced phosphorylation of <t>STAT1.</t> The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were left untreated or treated with IFN-β (100 ng/mL) for the indicated times before immunoblotting analysis with the indicated antibodies. (D) Effects of HTATSF1-deficiency on transcription of downstream genes induced by IFN-β. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were left untreated or treated with IFN-β (100 ng/mL) for 2 h before RT-qPCR analysis to measure mRNA levels of the indicated genes. Data shown are mean ± SEM ( n = 3 technical replicates) from one representative experiment ( (A) , ( B) , (D) ), which were repeated for at least two times with similar results. n.s., not significant; ∗∗, P < 0.01 (unpaired t -test).
    P Stat1 Y701, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 353 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    p stat1 y701 - by Bioz Stars, 2026-02
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    Images

    1) Product Images from "HTATSF1 regulates innate antiviral immune response by orchestrating TRAF3-IRF3 and TRAF6-NF-κB pathways"

    Article Title: HTATSF1 regulates innate antiviral immune response by orchestrating TRAF3-IRF3 and TRAF6-NF-κB pathways

    Journal: Cell Insight

    doi: 10.1016/j.cellin.2025.100294

    HTATSF1 mediates viral nucleic acid- but not IFN-β-triggered signaling. (A) Effects of HTATSF1-deficiency on transcription of downstream genes induced by viral nucleic acid mimics. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were untransfected or transfected with HT-DNA (2 μg/mL) or poly(I:C) (2 μg/mL) for the indicated times before RT-qPCR analysis to measure mRNA levels of the indicated genes. (B) Effects of HTATSF1-deficiency on transcription of downstream genes induced by cGAMP. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were left untreated or treated with 2′3′-cGAMP (40 nM) for the indicated times before RT-qPCR analysis to measure mRNA levels of the indicated genes. (C) Effects of HTATSF1-deficiency on IFN-β-induced phosphorylation of STAT1. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were left untreated or treated with IFN-β (100 ng/mL) for the indicated times before immunoblotting analysis with the indicated antibodies. (D) Effects of HTATSF1-deficiency on transcription of downstream genes induced by IFN-β. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were left untreated or treated with IFN-β (100 ng/mL) for 2 h before RT-qPCR analysis to measure mRNA levels of the indicated genes. Data shown are mean ± SEM ( n = 3 technical replicates) from one representative experiment ( (A) , ( B) , (D) ), which were repeated for at least two times with similar results. n.s., not significant; ∗∗, P < 0.01 (unpaired t -test).
    Figure Legend Snippet: HTATSF1 mediates viral nucleic acid- but not IFN-β-triggered signaling. (A) Effects of HTATSF1-deficiency on transcription of downstream genes induced by viral nucleic acid mimics. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were untransfected or transfected with HT-DNA (2 μg/mL) or poly(I:C) (2 μg/mL) for the indicated times before RT-qPCR analysis to measure mRNA levels of the indicated genes. (B) Effects of HTATSF1-deficiency on transcription of downstream genes induced by cGAMP. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were left untreated or treated with 2′3′-cGAMP (40 nM) for the indicated times before RT-qPCR analysis to measure mRNA levels of the indicated genes. (C) Effects of HTATSF1-deficiency on IFN-β-induced phosphorylation of STAT1. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were left untreated or treated with IFN-β (100 ng/mL) for the indicated times before immunoblotting analysis with the indicated antibodies. (D) Effects of HTATSF1-deficiency on transcription of downstream genes induced by IFN-β. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were left untreated or treated with IFN-β (100 ng/mL) for 2 h before RT-qPCR analysis to measure mRNA levels of the indicated genes. Data shown are mean ± SEM ( n = 3 technical replicates) from one representative experiment ( (A) , ( B) , (D) ), which were repeated for at least two times with similar results. n.s., not significant; ∗∗, P < 0.01 (unpaired t -test).

    Techniques Used: Control, Transfection, Quantitative RT-PCR, Phospho-proteomics, Western Blot

    HTATSF1 is important for HSV-1- or SeV-triggered phosphorylation of downstream signaling components. (A) Effects of HTATSF1-deficiency on HSV-1- or SeV-induced phosphorylation of TBK1, IRF3, and STAT1 in THP-1 cells. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were left uninfected or infected with HSV-1 (MOI = 1) or SeV (MOI = 1) for the indicated times before immunoblotting analysis with the indicated antibodies. (B) Effects of HTATSF1-deficiency on HSV-1- or SeV-induced phosphorylation of TBK1, IRF3, and STAT1 in BMDMs. Lyz2 -Cre; Htatsf1 fl/fl and Htatsf1 fl/fl BMDM cells (1 × 10 6 ) were left uninfected or infected with HSV-1 (MOI = 1) or SeV (MOI = 1) for the indicated times before immunoblotting analysis with the indicated antibodies.
    Figure Legend Snippet: HTATSF1 is important for HSV-1- or SeV-triggered phosphorylation of downstream signaling components. (A) Effects of HTATSF1-deficiency on HSV-1- or SeV-induced phosphorylation of TBK1, IRF3, and STAT1 in THP-1 cells. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were left uninfected or infected with HSV-1 (MOI = 1) or SeV (MOI = 1) for the indicated times before immunoblotting analysis with the indicated antibodies. (B) Effects of HTATSF1-deficiency on HSV-1- or SeV-induced phosphorylation of TBK1, IRF3, and STAT1 in BMDMs. Lyz2 -Cre; Htatsf1 fl/fl and Htatsf1 fl/fl BMDM cells (1 × 10 6 ) were left uninfected or infected with HSV-1 (MOI = 1) or SeV (MOI = 1) for the indicated times before immunoblotting analysis with the indicated antibodies.

    Techniques Used: Phospho-proteomics, Control, Infection, Western Blot



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    HTATSF1 mediates viral nucleic acid- but not IFN-β-triggered signaling. (A) Effects of HTATSF1-deficiency on transcription of downstream genes induced by viral nucleic acid mimics. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were untransfected or transfected with HT-DNA (2 μg/mL) or poly(I:C) (2 μg/mL) for the indicated times before RT-qPCR analysis to measure mRNA levels of the indicated genes. (B) Effects of HTATSF1-deficiency on transcription of downstream genes induced by cGAMP. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were left untreated or treated with 2′3′-cGAMP (40 nM) for the indicated times before RT-qPCR analysis to measure mRNA levels of the indicated genes. (C) Effects of HTATSF1-deficiency on IFN-β-induced phosphorylation of <t>STAT1.</t> The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were left untreated or treated with IFN-β (100 ng/mL) for the indicated times before immunoblotting analysis with the indicated antibodies. (D) Effects of HTATSF1-deficiency on transcription of downstream genes induced by IFN-β. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were left untreated or treated with IFN-β (100 ng/mL) for 2 h before RT-qPCR analysis to measure mRNA levels of the indicated genes. Data shown are mean ± SEM ( n = 3 technical replicates) from one representative experiment ( (A) , ( B) , (D) ), which were repeated for at least two times with similar results. n.s., not significant; ∗∗, P < 0.01 (unpaired t -test).
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    Image Search Results


    HTATSF1 mediates viral nucleic acid- but not IFN-β-triggered signaling. (A) Effects of HTATSF1-deficiency on transcription of downstream genes induced by viral nucleic acid mimics. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were untransfected or transfected with HT-DNA (2 μg/mL) or poly(I:C) (2 μg/mL) for the indicated times before RT-qPCR analysis to measure mRNA levels of the indicated genes. (B) Effects of HTATSF1-deficiency on transcription of downstream genes induced by cGAMP. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were left untreated or treated with 2′3′-cGAMP (40 nM) for the indicated times before RT-qPCR analysis to measure mRNA levels of the indicated genes. (C) Effects of HTATSF1-deficiency on IFN-β-induced phosphorylation of STAT1. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were left untreated or treated with IFN-β (100 ng/mL) for the indicated times before immunoblotting analysis with the indicated antibodies. (D) Effects of HTATSF1-deficiency on transcription of downstream genes induced by IFN-β. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were left untreated or treated with IFN-β (100 ng/mL) for 2 h before RT-qPCR analysis to measure mRNA levels of the indicated genes. Data shown are mean ± SEM ( n = 3 technical replicates) from one representative experiment ( (A) , ( B) , (D) ), which were repeated for at least two times with similar results. n.s., not significant; ∗∗, P < 0.01 (unpaired t -test).

    Journal: Cell Insight

    Article Title: HTATSF1 regulates innate antiviral immune response by orchestrating TRAF3-IRF3 and TRAF6-NF-κB pathways

    doi: 10.1016/j.cellin.2025.100294

    Figure Lengend Snippet: HTATSF1 mediates viral nucleic acid- but not IFN-β-triggered signaling. (A) Effects of HTATSF1-deficiency on transcription of downstream genes induced by viral nucleic acid mimics. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were untransfected or transfected with HT-DNA (2 μg/mL) or poly(I:C) (2 μg/mL) for the indicated times before RT-qPCR analysis to measure mRNA levels of the indicated genes. (B) Effects of HTATSF1-deficiency on transcription of downstream genes induced by cGAMP. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were left untreated or treated with 2′3′-cGAMP (40 nM) for the indicated times before RT-qPCR analysis to measure mRNA levels of the indicated genes. (C) Effects of HTATSF1-deficiency on IFN-β-induced phosphorylation of STAT1. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were left untreated or treated with IFN-β (100 ng/mL) for the indicated times before immunoblotting analysis with the indicated antibodies. (D) Effects of HTATSF1-deficiency on transcription of downstream genes induced by IFN-β. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were left untreated or treated with IFN-β (100 ng/mL) for 2 h before RT-qPCR analysis to measure mRNA levels of the indicated genes. Data shown are mean ± SEM ( n = 3 technical replicates) from one representative experiment ( (A) , ( B) , (D) ), which were repeated for at least two times with similar results. n.s., not significant; ∗∗, P < 0.01 (unpaired t -test).

    Article Snippet: Antibodies against HA (TA180128) (OriGene); Flag (F3165) and β-actin (A2228) (Sigma); p-TBK1 S172 (ab109272), TBK1 (ab40676), p-IRF3 S386 (ab76493), TAK1 (ab109526), TRAF6 (ab33915), p65 (ab7970), ubiquitin (ab7254), K48-linkage specific polyubiquitin (ab140601) and K63-linkage specific polyubiquitin (ab179434) (Abcam); IRF3 (sc-33641) and STAT1 (SC-417) (Santa Cruz Biotechnology); Myc (5605), p-IRF3 S396 (4947), p-STAT1 Y701 (9167), TRAF3 (4729), p-TAK1 T184/187 (4508), p-IκBα S32/36 (9246), IκBα (9242), p-IKKα/β S176/177 (2078), IKKβ (2370), and p-p65 S536 (3033) (Cell Signaling Technology), HTATSF1 (20805-1-AP) and HECTD3 (11487-1-AP) (Proteintech) were purchased from the indicated companies.

    Techniques: Control, Transfection, Quantitative RT-PCR, Phospho-proteomics, Western Blot

    HTATSF1 is important for HSV-1- or SeV-triggered phosphorylation of downstream signaling components. (A) Effects of HTATSF1-deficiency on HSV-1- or SeV-induced phosphorylation of TBK1, IRF3, and STAT1 in THP-1 cells. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were left uninfected or infected with HSV-1 (MOI = 1) or SeV (MOI = 1) for the indicated times before immunoblotting analysis with the indicated antibodies. (B) Effects of HTATSF1-deficiency on HSV-1- or SeV-induced phosphorylation of TBK1, IRF3, and STAT1 in BMDMs. Lyz2 -Cre; Htatsf1 fl/fl and Htatsf1 fl/fl BMDM cells (1 × 10 6 ) were left uninfected or infected with HSV-1 (MOI = 1) or SeV (MOI = 1) for the indicated times before immunoblotting analysis with the indicated antibodies.

    Journal: Cell Insight

    Article Title: HTATSF1 regulates innate antiviral immune response by orchestrating TRAF3-IRF3 and TRAF6-NF-κB pathways

    doi: 10.1016/j.cellin.2025.100294

    Figure Lengend Snippet: HTATSF1 is important for HSV-1- or SeV-triggered phosphorylation of downstream signaling components. (A) Effects of HTATSF1-deficiency on HSV-1- or SeV-induced phosphorylation of TBK1, IRF3, and STAT1 in THP-1 cells. The control (g NC ) and HTATSF1-deficient (g HTATSF1 ) THP-1 cells (1 × 10 6 ) were left uninfected or infected with HSV-1 (MOI = 1) or SeV (MOI = 1) for the indicated times before immunoblotting analysis with the indicated antibodies. (B) Effects of HTATSF1-deficiency on HSV-1- or SeV-induced phosphorylation of TBK1, IRF3, and STAT1 in BMDMs. Lyz2 -Cre; Htatsf1 fl/fl and Htatsf1 fl/fl BMDM cells (1 × 10 6 ) were left uninfected or infected with HSV-1 (MOI = 1) or SeV (MOI = 1) for the indicated times before immunoblotting analysis with the indicated antibodies.

    Article Snippet: Antibodies against HA (TA180128) (OriGene); Flag (F3165) and β-actin (A2228) (Sigma); p-TBK1 S172 (ab109272), TBK1 (ab40676), p-IRF3 S386 (ab76493), TAK1 (ab109526), TRAF6 (ab33915), p65 (ab7970), ubiquitin (ab7254), K48-linkage specific polyubiquitin (ab140601) and K63-linkage specific polyubiquitin (ab179434) (Abcam); IRF3 (sc-33641) and STAT1 (SC-417) (Santa Cruz Biotechnology); Myc (5605), p-IRF3 S396 (4947), p-STAT1 Y701 (9167), TRAF3 (4729), p-TAK1 T184/187 (4508), p-IκBα S32/36 (9246), IκBα (9242), p-IKKα/β S176/177 (2078), IKKβ (2370), and p-p65 S536 (3033) (Cell Signaling Technology), HTATSF1 (20805-1-AP) and HECTD3 (11487-1-AP) (Proteintech) were purchased from the indicated companies.

    Techniques: Phospho-proteomics, Control, Infection, Western Blot

    CXCL12 and its receptor CXCR4 were expressed and localized in the ovary, with their binding activating the JAK/STAT signaling pathway. (A) Immunofluorescence staining of ovarian follicles revealed that CXCL12 was co-localized with its receptor CXCR4 in ovarian follicles. (B) CXCL12 overexpression significantly promoted the expression of CXCR4 , JAK2 and STAT1 . (C) Knocking down CXCL12 significantly inhibited the expression of CXCR4 , JAK2 and STAT1 . (D) CXCL12 overexpression in GCs promoted the protein expression of CXCR4, JAK2 and STAT1 as well as the phosphorylation of JAK2 and STAT1. When CXCL12 was knocked down, the results were reversed. (E) MSX-122 inhibitor-based treatment further confirmed that CXCL12 promoted the total protein and phosphorylation levels of JAK2 and STAT1 (The t test was used for the above analyses comparing two individual samples. * p<0.05; ** p<0.01; *** p<0.001).

    Journal: Animal Bioscience

    Article Title: Transcriptomic analysis identifies CXCL12 as a novel candidate gene for litter size in rabbits

    doi: 10.5713/ab.24.0640

    Figure Lengend Snippet: CXCL12 and its receptor CXCR4 were expressed and localized in the ovary, with their binding activating the JAK/STAT signaling pathway. (A) Immunofluorescence staining of ovarian follicles revealed that CXCL12 was co-localized with its receptor CXCR4 in ovarian follicles. (B) CXCL12 overexpression significantly promoted the expression of CXCR4 , JAK2 and STAT1 . (C) Knocking down CXCL12 significantly inhibited the expression of CXCR4 , JAK2 and STAT1 . (D) CXCL12 overexpression in GCs promoted the protein expression of CXCR4, JAK2 and STAT1 as well as the phosphorylation of JAK2 and STAT1. When CXCL12 was knocked down, the results were reversed. (E) MSX-122 inhibitor-based treatment further confirmed that CXCL12 promoted the total protein and phosphorylation levels of JAK2 and STAT1 (The t test was used for the above analyses comparing two individual samples. * p<0.05; ** p<0.01; *** p<0.001).

    Article Snippet: Protein detection was achieved using the following antibodies: anti-CCND1 mouse monoclonal antibody (1:250, Proteintech), anti-PCNA rabbit polyclonal antibody (1:250, Proteintech), anti-Bcl2 rabbit polyclonal antibody (1:250, Proteintech), anti-Bax rabbit polyclonal antibody (1:250, Proteintech), anti-CITED1 rabbit polyclonal antibody (1:50, Proteintech), anti-WNT10B mouse monoclonal polyclonal antibody (1:250, Proteintech), anti-CXCR4 mouse monoclonal polyclonal antibody (1:250, Proteintech), anti-phospho-JAK2 rabbit monoclonal polyclonal antibody (1:250, Abcam, Cambridge, UK), anti-JAK2 rabbit monoclonal polyclonal antibody (1:250, Abcam), anti-phospho-STAT1 rabbit polyclonal antibody (1:250, Proteintech), anti-STAT1 rabbit polyclonal antibody (1:250, Proteintech), anti-GAPDH mouse monoclonal antibody (1:2,500, Proteintech), 1:1,000 goat anti-rabbit secondary antibody IgG (Proteintech) and 1:1,000 goat anti-mouse secondary antibody IgG (Proteintech).

    Techniques: Binding Assay, Immunofluorescence, Staining, Over Expression, Expressing, Phospho-proteomics

    CXCL12 and its receptor CXCR4 were expressed and localized in the ovary, with their binding activating the JAK/STAT signaling pathway. (A) Immunofluorescence staining of ovarian follicles revealed that CXCL12 was co-localized with its receptor CXCR4 in ovarian follicles. (B) CXCL12 overexpression significantly promoted the expression of CXCR4 , JAK2 and STAT1 . (C) Knocking down CXCL12 significantly inhibited the expression of CXCR4 , JAK2 and STAT1 . (D) CXCL12 overexpression in GCs promoted the protein expression of CXCR4, JAK2 and STAT1 as well as the phosphorylation of JAK2 and STAT1. When CXCL12 was knocked down, the results were reversed. (E) MSX-122 inhibitor-based treatment further confirmed that CXCL12 promoted the total protein and phosphorylation levels of JAK2 and STAT1 (The t test was used for the above analyses comparing two individual samples. * p<0.05; ** p<0.01; *** p<0.001).

    Journal: Animal Bioscience

    Article Title: Transcriptomic analysis identifies CXCL12 as a novel candidate gene for litter size in rabbits

    doi: 10.5713/ab.24.0640

    Figure Lengend Snippet: CXCL12 and its receptor CXCR4 were expressed and localized in the ovary, with their binding activating the JAK/STAT signaling pathway. (A) Immunofluorescence staining of ovarian follicles revealed that CXCL12 was co-localized with its receptor CXCR4 in ovarian follicles. (B) CXCL12 overexpression significantly promoted the expression of CXCR4 , JAK2 and STAT1 . (C) Knocking down CXCL12 significantly inhibited the expression of CXCR4 , JAK2 and STAT1 . (D) CXCL12 overexpression in GCs promoted the protein expression of CXCR4, JAK2 and STAT1 as well as the phosphorylation of JAK2 and STAT1. When CXCL12 was knocked down, the results were reversed. (E) MSX-122 inhibitor-based treatment further confirmed that CXCL12 promoted the total protein and phosphorylation levels of JAK2 and STAT1 (The t test was used for the above analyses comparing two individual samples. * p<0.05; ** p<0.01; *** p<0.001).

    Article Snippet: Protein detection was achieved using the following antibodies: anti-CCND1 mouse monoclonal antibody (1:250, Proteintech), anti-PCNA rabbit polyclonal antibody (1:250, Proteintech), anti-Bcl2 rabbit polyclonal antibody (1:250, Proteintech), anti-Bax rabbit polyclonal antibody (1:250, Proteintech), anti-CITED1 rabbit polyclonal antibody (1:50, Proteintech), anti-WNT10B mouse monoclonal polyclonal antibody (1:250, Proteintech), anti-CXCR4 mouse monoclonal polyclonal antibody (1:250, Proteintech), anti-phospho-JAK2 rabbit monoclonal polyclonal antibody (1:250, Abcam, Cambridge, UK), anti-JAK2 rabbit monoclonal polyclonal antibody (1:250, Abcam), anti-phospho-STAT1 rabbit polyclonal antibody (1:250, Proteintech), anti-STAT1 rabbit polyclonal antibody (1:250, Proteintech), anti-GAPDH mouse monoclonal antibody (1:2,500, Proteintech), 1:1,000 goat anti-rabbit secondary antibody IgG (Proteintech) and 1:1,000 goat anti-mouse secondary antibody IgG (Proteintech).

    Techniques: Binding Assay, Immunofluorescence, Staining, Over Expression, Expressing, Phospho-proteomics