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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 66 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti stat2 antibody/product/Proteintech
Average 94 stars, based on 66 article reviews

anti stat2 antibody - by Bioz Stars, 2026-03

94/100 stars

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1) Product Images from "STAT2 Promotes Tumor Growth in Colorectal Cancer Independent of Type I IFN Receptor Signaling"

Article Title: STAT2 Promotes Tumor Growth in Colorectal Cancer Independent of Type I IFN Receptor Signaling

Journal: Current Oncology

doi: 10.3390/curroncol32120707

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.

Figure Legend 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.

Techniques Used: 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.

Figure Legend 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.

Techniques Used: 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.

Figure Legend 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.

Techniques Used: 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.

Figure Legend 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.

Techniques Used: 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.

Figure Legend 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.

Techniques Used: In Vitro, MTS Assay, Injection

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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

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.

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.

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.

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.

Techniques: In Vitro, MTS Assay, Injection

Effects of LF-C3GNPs on LTA-induced inflammation in HC11 cells. (A) Schematic diagram of cell culture protocol, LTA-induced inflammation in HC11 pretreated with LF-C3GNPs, the experimental verification. ( B-D) Cell viability of LF, C3G, and LF-C3GNPs. (E – J) mRNA (E – I) and protein (J) expression levels of MPO, TNF-α, IL-1β, IL-6, and SOCS3 in HC11 cells. (K) Immunofluorescence staining of TNF-α. Scale bar: 50 μm. (L – O) mRNA (L – N) and protein (O) expression levels of phosphorylated STATs (p-STAT1, p-STAT2, and p-STAT3) and STAT1, STAT2, and STAT3 in HC11 cells after different treatments. The data are presented as mean ± standard deviation (SD) from three independent replicates. Statistical significance is designated as # p<0.05 compared to the untreated control group; ∗ p<0.05 , ∗∗ p<0.01 , ∗∗∗ p<0.001 , and ∗∗∗∗ p<0.0001 relative to the LTA-treated groups.

Journal: Materials Today Bio

Article Title: Lactoferrin-cyanidin-3-glucoside nanoparticles alleviate inflammation and oxidative stress via Sesn2/Nrf2 activation in mastitis

doi: 10.1016/j.mtbio.2025.102491

Figure Lengend Snippet: Effects of LF-C3GNPs on LTA-induced inflammation in HC11 cells. (A) Schematic diagram of cell culture protocol, LTA-induced inflammation in HC11 pretreated with LF-C3GNPs, the experimental verification. ( B-D) Cell viability of LF, C3G, and LF-C3GNPs. (E – J) mRNA (E – I) and protein (J) expression levels of MPO, TNF-α, IL-1β, IL-6, and SOCS3 in HC11 cells. (K) Immunofluorescence staining of TNF-α. Scale bar: 50 μm. (L – O) mRNA (L – N) and protein (O) expression levels of phosphorylated STATs (p-STAT1, p-STAT2, and p-STAT3) and STAT1, STAT2, and STAT3 in HC11 cells after different treatments. The data are presented as mean ± standard deviation (SD) from three independent replicates. Statistical significance is designated as # p<0.05 compared to the untreated control group; ∗ p<0.05 , ∗∗ p<0.01 , ∗∗∗ p<0.001 , and ∗∗∗∗ p<0.0001 relative to the LTA-treated groups.

Article Snippet: Antibodies IL-1β (16806-1-AP), STAT2 (16674-1-AP), SLC7A11 (26864-1-AP), GAPDH (60004-1-Ig), Nrf2 (16396-1-AP), HO-1 (10701-1-AP), Keap1 (10503-2-AP), NQO1 (11451-1-AP), MPO (22225-1-AP), SOCS3 (14025-1-AP), and SESN2 (66297-1-Ig) were obtained from Proteintech BioTechnology (Wuhan, China).

Techniques: Cell Culture, Expressing, Immunofluorescence, Staining, Standard Deviation, Control

LF-C3GNPs preferentially target STAT2/3 rather than STAT1 in LTA-stimulated cells. (A – G) Western blot and quantification showing the effects of LF-C3GNPs and STAT1 overexpression (Oe-STAT1) on STAT1/p-STAT1 and downstream inflammatory mediators (MPO, TNF-α, IL-1β, IL-6) in LTA-stimulated cells. (H) Heatmap of relative mRNA expression of genes. (I – O) Western blot and quantification demonstrating the effects of LF-C3GNPs and STAT2 overexpression (Oe-STAT2) on STAT2/p-STAT2 and downstream mediators. (P) Heatmap of relative mRNA expression of genes. (Q – W) Western blot and quantification showing the effects of LF-C3GNPs and STAT3 overexpression (Oe-STAT3) on STAT3/p-STAT3 and downstream mediators. (X) Heatmap of relative mRNA expression of genes. Data are presented as mean ± SD (n = 3). ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001 ; ns, not significant.

Journal: Materials Today Bio

Article Title: Lactoferrin-cyanidin-3-glucoside nanoparticles alleviate inflammation and oxidative stress via Sesn2/Nrf2 activation in mastitis

doi: 10.1016/j.mtbio.2025.102491

Figure Lengend Snippet: LF-C3GNPs preferentially target STAT2/3 rather than STAT1 in LTA-stimulated cells. (A – G) Western blot and quantification showing the effects of LF-C3GNPs and STAT1 overexpression (Oe-STAT1) on STAT1/p-STAT1 and downstream inflammatory mediators (MPO, TNF-α, IL-1β, IL-6) in LTA-stimulated cells. (H) Heatmap of relative mRNA expression of genes. (I – O) Western blot and quantification demonstrating the effects of LF-C3GNPs and STAT2 overexpression (Oe-STAT2) on STAT2/p-STAT2 and downstream mediators. (P) Heatmap of relative mRNA expression of genes. (Q – W) Western blot and quantification showing the effects of LF-C3GNPs and STAT3 overexpression (Oe-STAT3) on STAT3/p-STAT3 and downstream mediators. (X) Heatmap of relative mRNA expression of genes. Data are presented as mean ± SD (n = 3). ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001 ; ns, not significant.

Techniques: Western Blot, Over Expression, Expressing

Effects of LF-C3GNPs on S. aureus -induced inflammation in mice. (A) Schematic diagram of mastitis modeling and LF-C3GNPs pre-administration in S. aureus -induced mastitis in mice. (B) H&E assay changes of S. aureus -infected mammary tissues in different groups. Scale bar: 500 μm. (C) Bacterial colony-forming unit (CFU) on agar plates and (D) quantification of CFU after different treatment groups. (E) Heatmap quantification and (F) proteins expression levels of MPO, TNF-α, IL-1β, IL-6, and SOCS3 in infected mice CFU after different treatment groups. (G) Immunofluorescence staining and (H) quantification of TNF-α. Scale bar: 200 μm. (I – K) mRNA and (L) Protein expression levels of phosphorylated STATs (p-STAT1, p-STAT2, and p-STAT3) and STAT1, STAT2, and STAT3 in infected mice. Mean ± SD; # p<0.05 compared to the untreated control group; ∗ p<0.05 , ∗∗ p<0.01 , ∗∗∗ p<0.001 , and ∗∗∗∗ p<0.0001 relative to the S. aureus -treated groups.

Journal: Materials Today Bio

Article Title: Lactoferrin-cyanidin-3-glucoside nanoparticles alleviate inflammation and oxidative stress via Sesn2/Nrf2 activation in mastitis

doi: 10.1016/j.mtbio.2025.102491

Figure Lengend Snippet: Effects of LF-C3GNPs on S. aureus -induced inflammation in mice. (A) Schematic diagram of mastitis modeling and LF-C3GNPs pre-administration in S. aureus -induced mastitis in mice. (B) H&E assay changes of S. aureus -infected mammary tissues in different groups. Scale bar: 500 μm. (C) Bacterial colony-forming unit (CFU) on agar plates and (D) quantification of CFU after different treatment groups. (E) Heatmap quantification and (F) proteins expression levels of MPO, TNF-α, IL-1β, IL-6, and SOCS3 in infected mice CFU after different treatment groups. (G) Immunofluorescence staining and (H) quantification of TNF-α. Scale bar: 200 μm. (I – K) mRNA and (L) Protein expression levels of phosphorylated STATs (p-STAT1, p-STAT2, and p-STAT3) and STAT1, STAT2, and STAT3 in infected mice. Mean ± SD; # p<0.05 compared to the untreated control group; ∗ p<0.05 , ∗∗ p<0.01 , ∗∗∗ p<0.001 , and ∗∗∗∗ p<0.0001 relative to the S. aureus -treated groups.

Techniques: Infection, Expressing, Immunofluorescence, Staining, Control

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1) Product Images from "STAT2 Promotes Tumor Growth in Colorectal Cancer Independent of Type I IFN Receptor Signaling"

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