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ab against p stat3 y705  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc ab against p stat3 y705
    Ab Against P Stat3 Y705, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 3692 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ab against p stat3 y705/product/Cell Signaling Technology Inc
    Average 98 stars, based on 3692 article reviews
    ab against p stat3 y705 - by Bioz Stars, 2026-06
    98/100 stars

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    Image Search Results


    Background characteristics of the study groups

    Journal: Immune Network

    Article Title: IL-17 Imbalance Promotes the Pyroptosis in Immune-Mediated Liver Injury Through STAT3-IFI16 Axis

    doi: 10.4110/in.2023.23.e46

    Figure Lengend Snippet: Background characteristics of the study groups

    Article Snippet: Abs against STAT3 (Cat# GTX104616, 1:1,000) was purchase from GeneTex (Irvine, CA, USA), and IFI16 (Cat# ab169788, 1:1,000) and internal control GAPDH (Cat# ab181602, 1:5,000) were purchase from Abcam (Waltham, MA, USA).

    Techniques: Control, shRNA

    Primers used in this study

    Journal: Immune Network

    Article Title: IL-17 Imbalance Promotes the Pyroptosis in Immune-Mediated Liver Injury Through STAT3-IFI16 Axis

    doi: 10.4110/in.2023.23.e46

    Figure Lengend Snippet: Primers used in this study

    Article Snippet: Abs against STAT3 (Cat# GTX104616, 1:1,000) was purchase from GeneTex (Irvine, CA, USA), and IFI16 (Cat# ab169788, 1:1,000) and internal control GAPDH (Cat# ab181602, 1:5,000) were purchase from Abcam (Waltham, MA, USA).

    Techniques: Sequencing

    Control (n=3), cells were cultured without treatment; NC (n=3), cells were treated with 100 ng/ml of IL-17 recombinant protein for 24 h; IL-17 protein (n=3), cells were treated with 100 ng/ml of IL-17 recombinant protein for 24 h; STAT3-OE (n=3), cells were treated with 100 ng/ml of IL-17 recombinant protein for 24 h, followed by treatment with the short hairpin RNA lentivirus that up-regulated the expression of STAT3 for 48 h; si-STAT3 (n=3), cells were treated with 100 ng/ml of IL-17 recombinant protein for 24 h, followed by treatment with the short hairpin RNA lentivirus that down-regulated the expression of STAT3 for 48 h; si-NC (n=3), cells were treated with 100 ng/ml of IL-17 recombinant protein for 24 h, followed by treatment with negative scrambled shRNA lentivirus that unregulated the expression of STAT for 48 h; IL-17 nAbs (n=3), cells were treated with IL-17 nAb (1 μg/dish) for 24 h; IL-17 nAbs+STAT3-OE (n=3), cells were treated with IL-17 nAb (1 μg/dish) for 24 h, followed by treatment with the short hairpin RNA lentivirus that up-regulated the expression of STAT3 for 48 h. * p<0.05, ** p<0.01.

    Journal: Immune Network

    Article Title: IL-17 Imbalance Promotes the Pyroptosis in Immune-Mediated Liver Injury Through STAT3-IFI16 Axis

    doi: 10.4110/in.2023.23.e46

    Figure Lengend Snippet: Control (n=3), cells were cultured without treatment; NC (n=3), cells were treated with 100 ng/ml of IL-17 recombinant protein for 24 h; IL-17 protein (n=3), cells were treated with 100 ng/ml of IL-17 recombinant protein for 24 h; STAT3-OE (n=3), cells were treated with 100 ng/ml of IL-17 recombinant protein for 24 h, followed by treatment with the short hairpin RNA lentivirus that up-regulated the expression of STAT3 for 48 h; si-STAT3 (n=3), cells were treated with 100 ng/ml of IL-17 recombinant protein for 24 h, followed by treatment with the short hairpin RNA lentivirus that down-regulated the expression of STAT3 for 48 h; si-NC (n=3), cells were treated with 100 ng/ml of IL-17 recombinant protein for 24 h, followed by treatment with negative scrambled shRNA lentivirus that unregulated the expression of STAT for 48 h; IL-17 nAbs (n=3), cells were treated with IL-17 nAb (1 μg/dish) for 24 h; IL-17 nAbs+STAT3-OE (n=3), cells were treated with IL-17 nAb (1 μg/dish) for 24 h, followed by treatment with the short hairpin RNA lentivirus that up-regulated the expression of STAT3 for 48 h. * p<0.05, ** p<0.01.

    Article Snippet: Abs against STAT3 (Cat# GTX104616, 1:1,000) was purchase from GeneTex (Irvine, CA, USA), and IFI16 (Cat# ab169788, 1:1,000) and internal control GAPDH (Cat# ab181602, 1:5,000) were purchase from Abcam (Waltham, MA, USA).

    Techniques: Control, Cell Culture, Recombinant, shRNA, Expressing

    Control (n=3), cells were cultured without treatment; NC (n=3), cells were treated with 100 ng/ml of IL-17 recombinant protein for 24 h; IL-17 protein (n=3), cells were treated with 100 ng/ml of IL-17 recombinant protein for 24 h; STAT3-OE (n=3), cells were treated with 100 ng/ml of IL-17 recombinant protein for 24 h, followed by treatment with the short hairpin RNA lentivirus that up-regulated the expression of STAT3 for 48 h; si-STAT3 (n=3), cells were treated with 100 ng/ml of IL-17 recombinant protein for 24 h, followed by treatment with the short hairpin RNA lentivirus that down-regulated the expression of STAT3 for 48 h; si-NC (n=3), cells were treated with 100 ng/ml of IL-17 recombinant protein for 24 h, followed by treatment with negative scrambled shRNA lentivirus that unregulated the expression of STAT for 48 h; IL-17 nAbs (n=3), cells were treated with IL-17 nAb (1 μg/dish) for 24 h; IL-17 nAbs+STAT3-OE (n=3), cells were treated with IL-17 nAb (1 μg/dish) for 24 h, followed by treatment with the shortcytokines hairpin RNA lentivirus that up-regulated the expression of STAT3 for 48 h. ** p<0.01.

    Journal: Immune Network

    Article Title: IL-17 Imbalance Promotes the Pyroptosis in Immune-Mediated Liver Injury Through STAT3-IFI16 Axis

    doi: 10.4110/in.2023.23.e46

    Figure Lengend Snippet: Control (n=3), cells were cultured without treatment; NC (n=3), cells were treated with 100 ng/ml of IL-17 recombinant protein for 24 h; IL-17 protein (n=3), cells were treated with 100 ng/ml of IL-17 recombinant protein for 24 h; STAT3-OE (n=3), cells were treated with 100 ng/ml of IL-17 recombinant protein for 24 h, followed by treatment with the short hairpin RNA lentivirus that up-regulated the expression of STAT3 for 48 h; si-STAT3 (n=3), cells were treated with 100 ng/ml of IL-17 recombinant protein for 24 h, followed by treatment with the short hairpin RNA lentivirus that down-regulated the expression of STAT3 for 48 h; si-NC (n=3), cells were treated with 100 ng/ml of IL-17 recombinant protein for 24 h, followed by treatment with negative scrambled shRNA lentivirus that unregulated the expression of STAT for 48 h; IL-17 nAbs (n=3), cells were treated with IL-17 nAb (1 μg/dish) for 24 h; IL-17 nAbs+STAT3-OE (n=3), cells were treated with IL-17 nAb (1 μg/dish) for 24 h, followed by treatment with the shortcytokines hairpin RNA lentivirus that up-regulated the expression of STAT3 for 48 h. ** p<0.01.

    Article Snippet: Abs against STAT3 (Cat# GTX104616, 1:1,000) was purchase from GeneTex (Irvine, CA, USA), and IFI16 (Cat# ab169788, 1:1,000) and internal control GAPDH (Cat# ab181602, 1:5,000) were purchase from Abcam (Waltham, MA, USA).

    Techniques: Control, Cell Culture, Recombinant, shRNA, Expressing

    Model (n=6), mice were challenged with ConA at a dosage of 15 mg/kg; NC (n=6), mice were challenged with ConA at a dosage of 15 mg/kg; Control (n=6), mice were received an equal amount of 0.9% normal saline; IL-17 nAbs (n=6), mice were administrated with IL-17 nAb (1 μg/kg) 24 h before were challenged with ConA at a dosage of 15 mg/kg; STAT3-OE (n=6), mice were given the short hairpin RNA lentivirus that up-regulated the expression of STAT3 at 10 8 virus per mouse every day for 7 days before were challenged with ConA at a dosage of 15 mg/kg; si-STAT3 (n=6), mice were given the short hairpin RNA lentivirus that down-regulated the expression at 10 8 virus per mouse every day for 7 days before were challenged with ConA at a dosage of 15 mg/kg; si-NC (n=6), mice were given the negative scrambled shRNA lentivirus that unregulated the expression at 10 8 virus per mouse every day for 7 days before were challenged with ConA at a dosage of 15 mg/kg; IL-17 nAbs+STAT3-OE+ConA (n=6), mice were administrated with IL-17 nAb (1 μg/kg) for 24 h, then were given the short hairpin RNA lentivirus that up-regulated the expression of STAT3 at 10 8 virus per mouse every day for 7 days before were challenged with ConA at a dosage of 15 mg/kg; STAT3-OE+ConA (n=6), mice were given the short hairpin RNA lentivirus that up-regulated the expression of STAT3 at 10 8 virus per mouse every day for 7 days before were challenged with ConA at a dosage of 15 mg/kg. * p<0.05, ** p<0.01.

    Journal: Immune Network

    Article Title: IL-17 Imbalance Promotes the Pyroptosis in Immune-Mediated Liver Injury Through STAT3-IFI16 Axis

    doi: 10.4110/in.2023.23.e46

    Figure Lengend Snippet: Model (n=6), mice were challenged with ConA at a dosage of 15 mg/kg; NC (n=6), mice were challenged with ConA at a dosage of 15 mg/kg; Control (n=6), mice were received an equal amount of 0.9% normal saline; IL-17 nAbs (n=6), mice were administrated with IL-17 nAb (1 μg/kg) 24 h before were challenged with ConA at a dosage of 15 mg/kg; STAT3-OE (n=6), mice were given the short hairpin RNA lentivirus that up-regulated the expression of STAT3 at 10 8 virus per mouse every day for 7 days before were challenged with ConA at a dosage of 15 mg/kg; si-STAT3 (n=6), mice were given the short hairpin RNA lentivirus that down-regulated the expression at 10 8 virus per mouse every day for 7 days before were challenged with ConA at a dosage of 15 mg/kg; si-NC (n=6), mice were given the negative scrambled shRNA lentivirus that unregulated the expression at 10 8 virus per mouse every day for 7 days before were challenged with ConA at a dosage of 15 mg/kg; IL-17 nAbs+STAT3-OE+ConA (n=6), mice were administrated with IL-17 nAb (1 μg/kg) for 24 h, then were given the short hairpin RNA lentivirus that up-regulated the expression of STAT3 at 10 8 virus per mouse every day for 7 days before were challenged with ConA at a dosage of 15 mg/kg; STAT3-OE+ConA (n=6), mice were given the short hairpin RNA lentivirus that up-regulated the expression of STAT3 at 10 8 virus per mouse every day for 7 days before were challenged with ConA at a dosage of 15 mg/kg. * p<0.05, ** p<0.01.

    Article Snippet: Abs against STAT3 (Cat# GTX104616, 1:1,000) was purchase from GeneTex (Irvine, CA, USA), and IFI16 (Cat# ab169788, 1:1,000) and internal control GAPDH (Cat# ab181602, 1:5,000) were purchase from Abcam (Waltham, MA, USA).

    Techniques: Control, Saline, shRNA, Expressing, Virus

    Model (n=6), mice were challenged with ConA at a dosage of 15 mg/kg; NC (n=6), mice were challenged with ConA at a dosage of 15 mg/kg; Control (n=6), mice were received an equal amount of 0.9% normal saline; IL-17 nAbs (n=6), mice were administrated with IL-17 nAb (1 μg/kg) 24 h before were challenged with ConA at a dosage of 15 mg/kg; STAT3-OE (n=6), mice were given the short hairpin RNA lentivirus that up-regulated the expression of STAT3 at 10 8 virus per mouse every day for 7 days before were challenged with ConA at a dosage of 15 mg/kg; si-STAT3 (n=6), mice were given the short hairpin RNA lentivirus that down-regulated the expression at 10 8 virus per mouse every day for 7 days before were challenged with ConA at a dosage of 15 mg/kg; si-NC (n=6), negative scrambled shRNA lentivirus that unregulated the expression of STAT was given at 10 8 virus per mouse every day for 7 days before were challenged with ConA at a dosage of 15 mg/kg; IL-17 nAbs+STAT3-OE+ConA (n=6), mice were administrated with IL-17 nAb (1 μg/kg) for 24 h, then were given the short hairpin RNA lentivirus that up-regulated the expression of STAT3 at 10 8 virus per mouse every day for 7 days before were challenged with ConA at a dosage of 15 mg/kg; STAT3-OE+ConA (n=6), mice were given the short hairpin RNA lentivirus that up-regulated the expression of STAT3 at 10 8 virus per mouse every day for 7 days before were challenged with ConA at a dosage of 15 mg/kg. * p<0.05, ** p<0.01.

    Journal: Immune Network

    Article Title: IL-17 Imbalance Promotes the Pyroptosis in Immune-Mediated Liver Injury Through STAT3-IFI16 Axis

    doi: 10.4110/in.2023.23.e46

    Figure Lengend Snippet: Model (n=6), mice were challenged with ConA at a dosage of 15 mg/kg; NC (n=6), mice were challenged with ConA at a dosage of 15 mg/kg; Control (n=6), mice were received an equal amount of 0.9% normal saline; IL-17 nAbs (n=6), mice were administrated with IL-17 nAb (1 μg/kg) 24 h before were challenged with ConA at a dosage of 15 mg/kg; STAT3-OE (n=6), mice were given the short hairpin RNA lentivirus that up-regulated the expression of STAT3 at 10 8 virus per mouse every day for 7 days before were challenged with ConA at a dosage of 15 mg/kg; si-STAT3 (n=6), mice were given the short hairpin RNA lentivirus that down-regulated the expression at 10 8 virus per mouse every day for 7 days before were challenged with ConA at a dosage of 15 mg/kg; si-NC (n=6), negative scrambled shRNA lentivirus that unregulated the expression of STAT was given at 10 8 virus per mouse every day for 7 days before were challenged with ConA at a dosage of 15 mg/kg; IL-17 nAbs+STAT3-OE+ConA (n=6), mice were administrated with IL-17 nAb (1 μg/kg) for 24 h, then were given the short hairpin RNA lentivirus that up-regulated the expression of STAT3 at 10 8 virus per mouse every day for 7 days before were challenged with ConA at a dosage of 15 mg/kg; STAT3-OE+ConA (n=6), mice were given the short hairpin RNA lentivirus that up-regulated the expression of STAT3 at 10 8 virus per mouse every day for 7 days before were challenged with ConA at a dosage of 15 mg/kg. * p<0.05, ** p<0.01.

    Article Snippet: Abs against STAT3 (Cat# GTX104616, 1:1,000) was purchase from GeneTex (Irvine, CA, USA), and IFI16 (Cat# ab169788, 1:1,000) and internal control GAPDH (Cat# ab181602, 1:5,000) were purchase from Abcam (Waltham, MA, USA).

    Techniques: Control, Saline, shRNA, Expressing, Virus

    Figure 5. Mifepristone antagonizes LIFR and reduces STAT3 activation. (A) Mifepristone inhibition activity of LIFR/LIF binding accessed by a cell-free AlphaScreen assay. (B) STAT3 transactivation on HepG2 cells. Results are expressed as mean ± SEM of five samples per group.

    Journal: Cells

    Article Title: Repositioning Mifepristone as a Leukaemia Inhibitory Factor Receptor Antagonist for the Treatment of Pancreatic Adenocarcinoma.

    doi: 10.3390/cells11213482

    Figure Lengend Snippet: Figure 5. Mifepristone antagonizes LIFR and reduces STAT3 activation. (A) Mifepristone inhibition activity of LIFR/LIF binding accessed by a cell-free AlphaScreen assay. (B) STAT3 transactivation on HepG2 cells. Results are expressed as mean ± SEM of five samples per group.

    Article Snippet: Protein extracts were electrophoresed on 12% acrylamide Tris-Glycine gel (Invitrogen), blotted to the nitrocellulose membrane, and then incubated overnight with primary Abs against STAT3 (sc-8019 1:500; Santa Cruz Biotechnology) and phosho-Stat3 (GTX118000 1:1000; Genetex).

    Techniques: Activation Assay, Inhibition, Activity Assay, Binding Assay, Amplified Luminescent Proximity Homogenous Assay

    Figure 7. Mifepristone inhibits in vitro migration in STAT3-dependent signalling. (A) Relative mRNA expression of Vimentin and CXCR4. (B) Immunofluorescence analysis of Vimentin expression. (C) Scratch wound healing assay. MIA PaCa-2 cell monolayers were scraped in a straight line using a p200 pipette tip; then, they were left untreated or primed with LIF 10 ng/mL alone or in combination with mifepristone 10 or 20 µM and EC359 25 nM. The wound generated was captured at 0 and 48 h of incubation with the compounds above described. The images show cell migration at the two times point indicated. (D) Images of obtained points were analysed, measuring scraped area and its closure vs. the first time point at 0 h. Results are the mean ± SEM of three samples per group (* represents statistical significance versus NT, and # versus LIF, p < 0.05). (E) Analysis of STAT3 signalling pathway. Representative Western blot analysis of STAT3 and phospho-STAT3, proteins in MIA-PaCa-2 cells exposed to LIF (10 nM) alone or in combination with increasing concentration of mifepristone (10, 20, 50 µM) for 20 min. (F) Densitometric analysis demonstrating phospho-STAT3/STAT3 ratio.

    Journal: Cells

    Article Title: Repositioning Mifepristone as a Leukaemia Inhibitory Factor Receptor Antagonist for the Treatment of Pancreatic Adenocarcinoma.

    doi: 10.3390/cells11213482

    Figure Lengend Snippet: Figure 7. Mifepristone inhibits in vitro migration in STAT3-dependent signalling. (A) Relative mRNA expression of Vimentin and CXCR4. (B) Immunofluorescence analysis of Vimentin expression. (C) Scratch wound healing assay. MIA PaCa-2 cell monolayers were scraped in a straight line using a p200 pipette tip; then, they were left untreated or primed with LIF 10 ng/mL alone or in combination with mifepristone 10 or 20 µM and EC359 25 nM. The wound generated was captured at 0 and 48 h of incubation with the compounds above described. The images show cell migration at the two times point indicated. (D) Images of obtained points were analysed, measuring scraped area and its closure vs. the first time point at 0 h. Results are the mean ± SEM of three samples per group (* represents statistical significance versus NT, and # versus LIF, p < 0.05). (E) Analysis of STAT3 signalling pathway. Representative Western blot analysis of STAT3 and phospho-STAT3, proteins in MIA-PaCa-2 cells exposed to LIF (10 nM) alone or in combination with increasing concentration of mifepristone (10, 20, 50 µM) for 20 min. (F) Densitometric analysis demonstrating phospho-STAT3/STAT3 ratio.

    Article Snippet: Protein extracts were electrophoresed on 12% acrylamide Tris-Glycine gel (Invitrogen), blotted to the nitrocellulose membrane, and then incubated overnight with primary Abs against STAT3 (sc-8019 1:500; Santa Cruz Biotechnology) and phosho-Stat3 (GTX118000 1:1000; Genetex).

    Techniques: In Vitro, Migration, Expressing, Wound Healing Assay, Transferring, Generated, Incubation, Western Blot, Concentration Assay

    Representative Western blot analysis of A) LIFR, JAK1 and phospho-JAK1, STAT3 and phospho-STAT3, proteins in MKN45 exposed to LIF (10 nM) alone or in combination with EC359 (25 nM and 100 nM) for 20 minutes. GAPDH was used as loading control. B) Densitometric analysis demonstrating LIFR expression, phospho-JAK1/JAK1 and phospho-STAT3/STAT3 ratio. The blot shown is representative of another one showing the same pattern.

    Journal: bioRxiv

    Article Title: Next generation sequencing analysis of gastric cancer identifies the leukemia inhibitory factor receptor (LIFR) as a driving factor in gastric cancer progression and as a predictor of poor prognosis

    doi: 10.1101/2022.05.05.490785

    Figure Lengend Snippet: Representative Western blot analysis of A) LIFR, JAK1 and phospho-JAK1, STAT3 and phospho-STAT3, proteins in MKN45 exposed to LIF (10 nM) alone or in combination with EC359 (25 nM and 100 nM) for 20 minutes. GAPDH was used as loading control. B) Densitometric analysis demonstrating LIFR expression, phospho-JAK1/JAK1 and phospho-STAT3/STAT3 ratio. The blot shown is representative of another one showing the same pattern.

    Article Snippet: Protein extracts were electrophoresed on 12% acrylamide Tris-Glycine gel (Invitrogen), blotted to nitrocellulose membrane, and then incubated overnight with primary Abs against Jak1 (sc-7228 1:500; Santa Cruz Biotechnology), phospho-Jak1 (GTX25493 1:1000; Genetex), STAT3 (sc-8019 1:500; Santa Cruz Biotechnology), phosho-STAT3 (GTX118000 1:1000; Genetex), and GAPDH (bs2188R 1:1000; Bioss antibodies).

    Techniques: Western Blot, Control, Expressing