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Santa Cruz Biotechnology human stat2 crispr cas9 ko plasmid
<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.
Human Stat2 Crispr Cas9 Ko Plasmid, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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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: Human STAT2 CRISPR/Cas9 KO plasmid (cat#sc-417454) was purchased by Santa Cruz Biotechnology (Santa Cruz, CA, 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: Human STAT2 CRISPR/Cas9 KO plasmid (cat#sc-417454) was purchased by Santa Cruz Biotechnology (Santa Cruz, CA, 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: Human STAT2 CRISPR/Cas9 KO plasmid (cat#sc-417454) was purchased by Santa Cruz Biotechnology (Santa Cruz, CA, 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: Human STAT2 CRISPR/Cas9 KO plasmid (cat#sc-417454) was purchased by Santa Cruz Biotechnology (Santa Cruz, CA, 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: Human STAT2 CRISPR/Cas9 KO plasmid (cat#sc-417454) was purchased by Santa Cruz Biotechnology (Santa Cruz, CA, USA).

Techniques: In Vitro, MTS Assay, Injection