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p stat1 ![]() P Stat1, supplied by Proteintech, 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/p stat1/product/Proteintech Average 96 stars, based on 1 article reviews
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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),
Techniques: Control, Transfection, Quantitative RT-PCR, Phospho-proteomics, Western Blot
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),
Techniques: Phospho-proteomics, Control, Infection, Western Blot
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),
Techniques: Binding Assay, Immunofluorescence, Staining, Over Expression, Expressing, Phospho-proteomics
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),
Techniques: Binding Assay, Immunofluorescence, Staining, Over Expression, Expressing, Phospho-proteomics