stat2 Search Results


96
Cell Signaling Technology Inc anti stat2
Anti Stat2, 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
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96
Cell Signaling Technology Inc anti phospho stat2 tyr690
Anti Phospho Stat2 Tyr690, 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
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95
Cell Signaling Technology Inc rabbit anti phosphorylated stat2 tyr690
Rabbit Anti Phosphorylated Stat2 Tyr690, 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
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Cell Signaling Technology Inc anti ptyr 1000 monoclonal pool

Anti Ptyr 1000 Monoclonal Pool, 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
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94
Cell Signaling Technology Inc stat2
Fig. 3. The nuclear accumulation of STAT1 and <t>STAT2</t> 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.
Stat2, supplied by Cell Signaling Technology Inc, 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/product/stat2/pm19085955-54-5-24?v=Cell+Signaling+Technology+Inc
Average 94 stars, based on 1 article reviews
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95
Santa Cruz Biotechnology stat2
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 <t>STAT2</t> 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.
Stat2, supplied by Santa Cruz Biotechnology, 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/product/stat2/10__1074_slash_jbc__m109__054486-66-19-20?v=Santa+Cruz+Biotechnology
Average 95 stars, based on 1 article reviews
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94
Proteintech anti stat2 antibody
<t>STAT2</t> 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.
Anti Stat2 Antibody, supplied by Proteintech, 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/product/stat2/pmc12732172-70-3-16?v=Proteintech
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88
Santa Cruz Biotechnology sistat2
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 <t>(siSTAT2)</t> 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.
Sistat2, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 88/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/stat2/pmc04336497-105-10-28?v=Santa+Cruz+Biotechnology
Average 88 stars, based on 1 article reviews
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92
Cell Signaling Technology Inc 90740s
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 <t>(siSTAT2)</t> 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.
90740s, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/stat2/pm33027651-456-169-165?v=Cell+Signaling+Technology+Inc
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91
Rockland Immunochemicals rabbit anti phospho stat2 primary antibody
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 <t>(siSTAT2)</t> 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.
Rabbit Anti Phospho Stat2 Primary Antibody, supplied by Rockland Immunochemicals, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/stat2/pmc06854505-490-0-7?v=Rockland+Immunochemicals
Average 91 stars, based on 1 article reviews
rabbit anti phospho stat2 primary antibody - by Bioz Stars, 2026-08
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93
R&D Systems anti stat2
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 <t>(siSTAT2)</t> 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.
Anti Stat2, supplied by R&D Systems, 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/product/stat2/pmc09682998-189-45-49?v=R%26D+Systems
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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: Anti-pTYR-1000 monoclonal pool , CST , Cat#8954; RRID: AB_2687925.

Techniques: Virus, Recombinant, Phospho-proteomics, Mutagenesis, Enzyme-linked Immunosorbent Assay, cDNA Synthesis, Genome Wide, Mass Spectrometry, Cell Culture, Software

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.

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, STAT2, Jak1, Tyk2, phosphotyrosine 701- STAT1 (pY-STAT1), phosphotyrosine 690-STAT2 (pYSTAT2), phosphotyrosine 1022/1023-Jak1 (pY-Jak1), and phosphotyrosine 1054/1055-Tyk2 (pY-Tyk2) were from Cell Signaling Technology, Inc. (Danvers, MA).

Techniques: Transfection, Staining

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.

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, STAT2, Jak1, Tyk2, phosphotyrosine 701- STAT1 (pY-STAT1), phosphotyrosine 690-STAT2 (pYSTAT2), phosphotyrosine 1022/1023-Jak1 (pY-Jak1), and phosphotyrosine 1054/1055-Tyk2 (pY-Tyk2) were from Cell Signaling Technology, Inc. (Danvers, MA).

Techniques: Inhibition, Phospho-proteomics, Transfection, Cell Culture, Polyacrylamide Gel Electrophoresis, Control

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.

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 STAT2 (Santa Cruz), and 25 l of protein G magnetic beads overnight at 4 °C.

Techniques: Binding Assay, Virus, Infection, Expressing, Phospho-proteomics, Control

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.

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), anti-STAT2 antibody (cat##51075-2-AP), anti-STAT3 (cat#10253-2-AP), anti-β-tubulin (cat#10094-1-AP), and anti-β-Actin (cat#66009-1-Ig) were purchased from Proteintech (Rosemont, IL, USA.

Techniques: Expressing

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.

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), anti-STAT2 antibody (cat##51075-2-AP), anti-STAT3 (cat#10253-2-AP), anti-β-tubulin (cat#10094-1-AP), and anti-β-Actin (cat#66009-1-Ig) were purchased from Proteintech (Rosemont, IL, USA.

Techniques: Activation Assay, Western Blot, Knock-Out, Clone Assay

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.

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), anti-STAT2 antibody (cat##51075-2-AP), anti-STAT3 (cat#10253-2-AP), anti-β-tubulin (cat#10094-1-AP), and anti-β-Actin (cat#66009-1-Ig) were purchased from Proteintech (Rosemont, IL, USA.

Techniques: In Vitro, Injection, Over Expression, In Vivo

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.

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), anti-STAT2 antibody (cat##51075-2-AP), anti-STAT3 (cat#10253-2-AP), anti-β-tubulin (cat#10094-1-AP), and anti-β-Actin (cat#66009-1-Ig) were purchased from Proteintech (Rosemont, IL, USA.

Techniques: Western Blot, Phospho-proteomics, Expressing

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.

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), anti-STAT2 antibody (cat##51075-2-AP), anti-STAT3 (cat#10253-2-AP), anti-β-tubulin (cat#10094-1-AP), and anti-β-Actin (cat#66009-1-Ig) were purchased from Proteintech (Rosemont, IL, USA.

Techniques: In Vitro, MTS Assay, Injection

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.

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), siSTAT2 (cat# sc-29492), siIFNα (cat# sc-63324), siIRF-7 (cat# 38011) and siRNA negative control (cat# sc-37007) were purchased from Santa Cruz Biotechnology, and siBax and siNoxa were purchased from Thermo Fisher Scientific (Pittsburg, PA, USA).

Techniques: Knockdown, Expressing, Transfection, Western Blot, Control, Standard Deviation