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Image Search Results
Journal: Cell Reports
Article Title: A single amino acid in the Salmonella effector SarA/SteE triggers supraphysiological activation of STAT3 for anti-inflammatory gene expression
doi: 10.1016/j.celrep.2025.115530
Figure Lengend Snippet:
Article Snippet:
Techniques: Virus, Recombinant, Phospho-proteomics, Mutagenesis, Enzyme-linked Immunosorbent Assay, cDNA Synthesis, Genome Wide, Mass Spectrometry, Cell Culture, Software
Journal: Hepatology (Baltimore, Md.)
Article Title: Hepatitis delta virus inhibits alpha interferon signaling.
doi: 10.1002/hep.22654
Figure Lengend Snippet: Fig. 3. The nuclear accumulation of STAT1 and STAT2 in response to IFN- is inhibited in HDV-transfected cells. Normal cells (Huh-7) or cells transfected with HDV cDNA [Huh-7 pS- VL(D3)] were seeded on glass coverslips and treated with 1000 U/mL IFN- for 30 minutes. Cells were fixed with 4% paraformaldehyde, permeabilized with 0.2% Triton X-100, and stained with antisera to STAT1 (A) or STAT2 (B) and HDAg. Nuclei were counterstained with 4,6-diamidino-2-phenylindole (blue). Arrows point to cells successfully transfected with HDV.
Article Snippet: Rabbit polyclonal antibodies to STAT1,
Techniques: Transfection, Staining
Journal: Hepatology (Baltimore, Md.)
Article Title: Hepatitis delta virus inhibits alpha interferon signaling.
doi: 10.1002/hep.22654
Figure Lengend Snippet: Fig. 4. HDV inhibition of IFN-–induced tyrosine phosphorylation of STAT1 and STAT2. Normal cells (Huh-7) and cells transfected with HDV cDNA [Huh-7 pSVL(D3)] were cultured for 9 days and then treated with 1000 U/mL IFN- for 30 minutes or left untreated. Equal amounts of cell lysates were separated by sodium dodecyl sulfate polyacrylamide gel electrophoresis, transferred onto nitrocellulose membranes, and exam- ined with antibodies to phosphotyrosine 701-STAT1 (pY-STAT1), STAT1, phosphotyrosine 690-STAT2 (pY-STAT2), STAT2, p48, and HDAg. -Actin levels served as a loading control.
Article Snippet: Rabbit polyclonal antibodies to STAT1,
Techniques: Inhibition, Phospho-proteomics, Transfection, Cell Culture, Polyacrylamide Gel Electrophoresis, Control
Journal: Journal of Biological Chemistry
Article Title: Viral Induction of the Zinc Finger Antiviral Protein Is IRF3-dependent but NF-κB-independent
doi: 10.1074/jbc.m109.054486
Figure Lengend Snippet: FIGURE 7. Differential binding of IRF3 and STAT transcription factors to the hZAP promoter following virus infection or IFN stimulation. A, immu- noblot analysis of ISG56 expression and phosphorylation status of STAT1 and STAT2 in HeLa cells following stimulation of IFN (500 units/ml) for 1 and 8 h or infection with SeV (100 HAU/ml) for 16 h. Actin blot was shown as a loading control. B, ChIP analyses of IRF3 and STAT binding to the ISRE1–2, ISRE3–5, and STAT V sites within hZAP promoter in HeLa cells mock treated, stimulated with IFN (400 units/ml) for 1 h, or infected with SeV (200 HAU/ml) for 8 h. The ChIP-enriched DNA levels analyzed by Q-PCR were normalized to input DNA, followed by subtraction of nonspecific binding determined with control IgG.
Article Snippet: Sheared chromatin was incubated with 2 g of control IgG (Active Motif) or specific antibody to IRF3, STAT1, or
Techniques: Binding Assay, Virus, Infection, Expressing, Phospho-proteomics, Control
Journal: Current Oncology
Article Title: STAT2 Promotes Tumor Growth in Colorectal Cancer Independent of Type I IFN Receptor Signaling
doi: 10.3390/curroncol32120707
Figure Lengend Snippet: STAT2 expression is elevated in colon tumors and correlates with reduced survival. Boxplots showing ( a ) STAT2 and ( c ) IFNAR1 mRNA expression are significantly higher in TCGA-COAD tumor tissues ( n = 286) compared with normal colon samples ( n = 41). ( b ) Kaplan–Meier survival curves for patients stratified by median STAT2 expression show reduced overall survival in the STAT2-high group. ( d ) STAT2-high tumors stratified by IFNAR1-high ( n = 56) and IFNAR-low ( n = 54) expression show no survival difference. Cox proportional hazards model was applied. Statistical significance; p ≤ 0.05.
Article Snippet: Anti-STAT1 antibody (Cat#10144-2-AP),
Techniques: Expressing
Journal: Current Oncology
Article Title: STAT2 Promotes Tumor Growth in Colorectal Cancer Independent of Type I IFN Receptor Signaling
doi: 10.3390/curroncol32120707
Figure Lengend Snippet: STAT3 activation is preserved in STAT2 KO tumor cells. ( a ) Western blots confirming basal levels of STAT1, STAT2, and STAT3 after deletion of STAT2 or IFNAR1 in knockout clones. ( b ) Time course analyses of phosphorylated STATs following IFN-I stimulation. ( c ) Impaired transcriptional response to IFN-I in both STAT2 KO and IFNAR1 KO cells. *** p ≤ 0.001; **** p ≤ 0.0001. ns, not statistically significant.
Article Snippet: Anti-STAT1 antibody (Cat#10144-2-AP),
Techniques: Activation Assay, Western Blot, Knock-Out, Clone Assay
Journal: Current Oncology
Article Title: STAT2 Promotes Tumor Growth in Colorectal Cancer Independent of Type I IFN Receptor Signaling
doi: 10.3390/curroncol32120707
Figure Lengend Snippet: STAT2 and IFNAR1 differentially regulate colon cancer cell proliferation and tumor growth. ( a ) In vitro MTS showing reduced proliferation of STAT2 KO compared with parental and IFNAR1 KO HCT116 cells over the course of 72 h. Data represent mean ± SEM from n = 3. ( b ) Growth of tumor xenografts in immunodeficient Rag1KO mice injected subcutaneously with parental, STAT2 KO, or IFNAR1 KO cells. ( c ) Overexpression of STAT2 in HCT116 cells enhanced tumor growth in vivo ( n = 5–8 mice per study). * p ≤ 0.05; **** p ≤ 0.0001. ns, not statistically significant. Results are from two combined independent experiments.
Article Snippet: Anti-STAT1 antibody (Cat#10144-2-AP),
Techniques: In Vitro, Injection, Over Expression, In Vivo
Journal: Current Oncology
Article Title: STAT2 Promotes Tumor Growth in Colorectal Cancer Independent of Type I IFN Receptor Signaling
doi: 10.3390/curroncol32120707
Figure Lengend Snippet: STAT2 signaling and IFN-I responsiveness in STAT2- and IFNAR1-deficient murine colon carcinoma cells. ( a ) Western blot analyses show IFN-I-stimulated phosphorylation of STAT1 and basal STAT1 expression in parental, STAT2 KO, and IFNAR1 KO MC38 cells. ( b ) IFN-I-stimulated phosphorylation of STAT3 and basal STAT2 expression analyzed by western blot analysis. ( c ) Impaired transcriptional responses in both KO cell lines after 6 and 24 h of IFN-β treatment. Data are shown as fold change from corresponding untreated cell genotype. * p ≤ 0.05; ** p ≤ 0.01; *** p ≤ 0.001. ns, not statistically significant.
Article Snippet: Anti-STAT1 antibody (Cat#10144-2-AP),
Techniques: Western Blot, Phospho-proteomics, Expressing
Journal: Current Oncology
Article Title: STAT2 Promotes Tumor Growth in Colorectal Cancer Independent of Type I IFN Receptor Signaling
doi: 10.3390/curroncol32120707
Figure Lengend Snippet: Loss of STAT2, but not IFNAR1, reduces proliferation and tumor growth in murine colon carcinoma cells. ( a ) In vitro MTS assay showing reduced proliferation of Stat2 KO tumor cells compared with parental and IFNAR1 KO cell lines over 72 h. Data represent mean ± SEM from n = 3. ( b , c ) Tumor growth curves of wild-type mice injected subcutaneously with parental, STAT2 KO, or IFNAR1 KO tumor cells. * p < 0.05; *** p < 0.001; **** p < 0.0001. Data are shown as mean ± SEM from n = 6–8 mice per group.
Article Snippet: Anti-STAT1 antibody (Cat#10144-2-AP),
Techniques: In Vitro, MTS Assay, Injection
Journal: Breast Cancer Research : BCR
Article Title: Targeting interferon response genes sensitizes aromatase inhibitor resistant breast cancer cells to estrogen-induced cell death
doi: 10.1186/s13058-014-0506-7
Figure Lengend Snippet: STAT1/STAT2 knockdown reduces IFITM1 and PLSCR1 expression. (A and B) MCF-7:5C cells were transfected with sicontrol (siCon), STAT1 siRNA (siSTAT1) or STAT2 siRNA (siSTAT2) and STAT1, STAT2, IFITM1 and PLSCR1 protein levels were assessed at 24 and 48 hours by Western blot analysis (left panels). Transfected cells were also treated with E 2 for an additional 24 and 48 hours and the above mentioned proteins were also measured (a and b, left panels). (A, B) Cell proliferation was measured in siSTAT1-knockdown and STAT2-knockdown cells in the presence or absence of E 2 by cell titer blue assay (right panels). Each value is a mean ± SD from three experiments. * P <0.05 or ** P <0.01 versus the control; # P <0.05 versus E 2 treatment. (C) MCF-7:5C cells were transfected with Bax siRNA (siBax) or Noxa siRNA (siNoxa) for 24 hours and then treated with 1 nM E 2 for an additional 24, 48 or 72 hours. Cells were harvested and analyzed for Bax, PLSCR1, Noxa, and IFITM1 protein expression by Western blot. Membranes were stripped and reprobed for β-actin, which was used as a loading control. E 2 , 17β-estradiol; IFITM1, interferon induced transmembrane protein1; PLSCR1, phospholipid scramblase 1; SD, standard deviation; STAT1,2, Signal transducer and activator of transcription 1,2.
Article Snippet: The siPLSCR1 (cat# sc-44028), siIFITM1 (cat# sc-44549), siSTAT1 (cat# sc-44123),
Techniques: Knockdown, Expressing, Transfection, Western Blot, Control, Standard Deviation