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Cell Signaling Technology Inc anti total stat3 igg
$Ethyl acetate fraction of CL-E inhibits IL-6-induced <t>STAT3</t> activation in Hep3B cells. (A) Hep3B cells stably expressing STAT3-responsive luciferase reporter (pSTAT3-Luc) were treated with IL-6 (10 ng/ml) for 12 h in the presence or absence of CL-E or an aqueous fraction of C. longa L. leaves extract at concentrations of 10, 30, and 60 µg/ml. Luciferase activity was measured according to the manufacturer's instructions. Data are presented as relative luciferase activity normalized to the untreated control. (B) Hep3B cells were seeded in 96-well plates and treated with each fraction for 24 h at the indicated concentrations. Cell viability was assessed using the MTT assay. Results are expressed as the percentage of viable cells relative to the untreated control. Data represent the mean ± SE (n≥3). * P<0.05 and ** P<0.01 vs. the IL-6 alone group; ## P<0.01 indicates a significant difference between the 10 and 60 µg/ml CL-E doses. CL-E, Curcuma longa L. extract; IL-6, interleukin 6; STAT3, signal transducer and activator of transcription 3.$
Anti Total Stat3 Igg, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/total+stat3/pmc12856536-31-5-21
Average 86 stars, based on 1 article reviews

anti total stat3 igg - by Bioz Stars, 2026-08

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1) Product Images from "Ethyl acetate fraction of Curcuma longa leaves suppresses IL-6-induced STAT3 activation via ERK signaling in Hep3B cells"

Article Title: Ethyl acetate fraction of Curcuma longa leaves suppresses IL-6-induced STAT3 activation via ERK signaling in Hep3B cells

Journal: Biomedical Reports

doi: 10.3892/br.2026.2108

$Ethyl acetate fraction of CL-E inhibits IL-6-induced STAT3 activation in Hep3B cells. (A) Hep3B cells stably expressing STAT3-responsive luciferase reporter (pSTAT3-Luc) were treated with IL-6 (10 ng/ml) for 12 h in the presence or absence of CL-E or an aqueous fraction of C. longa L. leaves extract at concentrations of 10, 30, and 60 µg/ml. Luciferase activity was measured according to the manufacturer's instructions. Data are presented as relative luciferase activity normalized to the untreated control. (B) Hep3B cells were seeded in 96-well plates and treated with each fraction for 24 h at the indicated concentrations. Cell viability was assessed using the MTT assay. Results are expressed as the percentage of viable cells relative to the untreated control. Data represent the mean ± SE (n≥3). * P<0.05 and ** P<0.01 vs. the IL-6 alone group; ## P<0.01 indicates a significant difference between the 10 and 60 µg/ml CL-E doses. CL-E, Curcuma longa L. extract; IL-6, interleukin 6; STAT3, signal transducer and activator of transcription 3.$
Figure Legend Snippet: Ethyl acetate fraction of CL-E inhibits IL-6-induced STAT3 activation in Hep3B cells. (A) Hep3B cells stably expressing STAT3-responsive luciferase reporter (pSTAT3-Luc) were treated with IL-6 (10 ng/ml) for 12 h in the presence or absence of CL-E or an aqueous fraction of C. longa L. leaves extract at concentrations of 10, 30, and 60 µg/ml. Luciferase activity was measured according to the manufacturer's instructions. Data are presented as relative luciferase activity normalized to the untreated control. (B) Hep3B cells were seeded in 96-well plates and treated with each fraction for 24 h at the indicated concentrations. Cell viability was assessed using the MTT assay. Results are expressed as the percentage of viable cells relative to the untreated control. Data represent the mean ± SE (n≥3). * P<0.05 and ** P<0.01 vs. the IL-6 alone group; ## P<0.01 indicates a significant difference between the 10 and 60 µg/ml CL-E doses. CL-E, Curcuma longa L. extract; IL-6, interleukin 6; STAT3, signal transducer and activator of transcription 3.

Techniques Used: Activation Assay, Stable Transfection, Expressing, Luciferase, Activity Assay, Control, MTT Assay

CL-E inhibits IL-6-induced STAT3 phosphorylation and nuclear translocation in Hep3B cells. (A) Hep3B cells were treated with IL-6 (10 ng/ml) for the indicated time periods (0-60 min). Total cell lysates were analyzed by western blotting using antibodies against P-STAT3 (Tyr705), P-STAT3 (Ser727) and total STAT3. (B) Cells were pretreated with the CL-E at 10, 30 and 60 µg/ml for 1 h and then stimulated with IL-6 (10 ng/ml) for 30 min. Proteins were extracted and analyzed by western blotting as described above. (C) STAT3 nuclear translocation was assessed by immunofluorescence microscopy. Hep3B cells were cultured on Nunc Lab-Tek II 8-well chamber slides and treated with IL-6 (10 ng/ml) for 4 h in the absence or presence of CL-E (60 µg/ml) or genistein (60 µM, positive control). Cells were fixed, permeabilized and stained with anti-STAT3 antibody followed by FITC-conjugated secondary antibody. Subcellular localization of STAT3 was visualized using fluorescence microscopy (Scale bar: 20 µm). CL-E, Curcuma longa L. extract; IL-6, interleukin 6; STAT3, signal transducer and activator of transcription 3; P-, phosphorylated.

Figure Legend Snippet: CL-E inhibits IL-6-induced STAT3 phosphorylation and nuclear translocation in Hep3B cells. (A) Hep3B cells were treated with IL-6 (10 ng/ml) for the indicated time periods (0-60 min). Total cell lysates were analyzed by western blotting using antibodies against P-STAT3 (Tyr705), P-STAT3 (Ser727) and total STAT3. (B) Cells were pretreated with the CL-E at 10, 30 and 60 µg/ml for 1 h and then stimulated with IL-6 (10 ng/ml) for 30 min. Proteins were extracted and analyzed by western blotting as described above. (C) STAT3 nuclear translocation was assessed by immunofluorescence microscopy. Hep3B cells were cultured on Nunc Lab-Tek II 8-well chamber slides and treated with IL-6 (10 ng/ml) for 4 h in the absence or presence of CL-E (60 µg/ml) or genistein (60 µM, positive control). Cells were fixed, permeabilized and stained with anti-STAT3 antibody followed by FITC-conjugated secondary antibody. Subcellular localization of STAT3 was visualized using fluorescence microscopy (Scale bar: 20 µm). CL-E, Curcuma longa L. extract; IL-6, interleukin 6; STAT3, signal transducer and activator of transcription 3; P-, phosphorylated.

Techniques Used: Phospho-proteomics, Translocation Assay, Western Blot, Immunofluorescence, Microscopy, Cell Culture, Positive Control, Staining, Fluorescence

ERK signaling pathway contributes to CL-E-mediated regulation of IL-6-induced STAT3 activation. (A) Hep3B cells were stimulated with IL-6 (10 ng/ml) for the indicated times (0, 5, 10, 30 and 60 min). Protein lysates underwent western blotting analysis using antibodies against P-ERK1/2 and total ERK1/2 to evaluate time-dependent ERK1/2 activation. (B) Cells were pretreated with CL-E at 10, 30 and 60 µg/ml for 1 h, followed by IL-6 stimulation (10 ng/ml) for 30 min. ERK1/2 phosphorylation was analyzed by western blotting analysis. (C) To investigate the role of ERK in STAT3 Ser727 phosphorylation, cells were treated with CL-E (60 µg/ml), PKC inhibitor bisindolylmaleimide II (20 µM), and/or the MEK1/2 inhibitor U0126 (20 µM) for 1 h in the absence of IL-6. Phosphorylation of STAT3 (Ser727) and total STAT3 were examined by western blotting analysis. (D) To determine whether ERK activation contributes to regulation of STAT3 Tyr705 phosphorylation, cells were pretreated with CL-E, U0126 and/or bisindolylmaleimide II (20 µM) for 1 h before IL-6 stimulation (10 ng/ml, 30 min). STAT3 Tyr705 phosphorylation was analyzed by western blotting. CL-E, Curcuma longa L. extract; IL-6, interleukin 6; STAT3, signal transducer and activator of transcription 3; P-, phosphorylated.

Figure Legend Snippet: ERK signaling pathway contributes to CL-E-mediated regulation of IL-6-induced STAT3 activation. (A) Hep3B cells were stimulated with IL-6 (10 ng/ml) for the indicated times (0, 5, 10, 30 and 60 min). Protein lysates underwent western blotting analysis using antibodies against P-ERK1/2 and total ERK1/2 to evaluate time-dependent ERK1/2 activation. (B) Cells were pretreated with CL-E at 10, 30 and 60 µg/ml for 1 h, followed by IL-6 stimulation (10 ng/ml) for 30 min. ERK1/2 phosphorylation was analyzed by western blotting analysis. (C) To investigate the role of ERK in STAT3 Ser727 phosphorylation, cells were treated with CL-E (60 µg/ml), PKC inhibitor bisindolylmaleimide II (20 µM), and/or the MEK1/2 inhibitor U0126 (20 µM) for 1 h in the absence of IL-6. Phosphorylation of STAT3 (Ser727) and total STAT3 were examined by western blotting analysis. (D) To determine whether ERK activation contributes to regulation of STAT3 Tyr705 phosphorylation, cells were pretreated with CL-E, U0126 and/or bisindolylmaleimide II (20 µM) for 1 h before IL-6 stimulation (10 ng/ml, 30 min). STAT3 Tyr705 phosphorylation was analyzed by western blotting. CL-E, Curcuma longa L. extract; IL-6, interleukin 6; STAT3, signal transducer and activator of transcription 3; P-, phosphorylated.

Techniques Used: Activation Assay, Western Blot, Phospho-proteomics

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Journal: Biomedical Reports

Article Title: Ethyl acetate fraction of Curcuma longa leaves suppresses IL-6-induced STAT3 activation via ERK signaling in Hep3B cells

doi: 10.3892/br.2026.2108

Figure Lengend Snippet: Ethyl acetate fraction of CL-E inhibits IL-6-induced STAT3 activation in Hep3B cells. (A) Hep3B cells stably expressing STAT3-responsive luciferase reporter (pSTAT3-Luc) were treated with IL-6 (10 ng/ml) for 12 h in the presence or absence of CL-E or an aqueous fraction of C. longa L. leaves extract at concentrations of 10, 30, and 60 µg/ml. Luciferase activity was measured according to the manufacturer's instructions. Data are presented as relative luciferase activity normalized to the untreated control. (B) Hep3B cells were seeded in 96-well plates and treated with each fraction for 24 h at the indicated concentrations. Cell viability was assessed using the MTT assay. Results are expressed as the percentage of viable cells relative to the untreated control. Data represent the mean ± SE (n≥3). * P<0.05 and ** P<0.01 vs. the IL-6 alone group; ## P<0.01 indicates a significant difference between the 10 and 60 µg/ml CL-E doses. CL-E, Curcuma longa L. extract; IL-6, interleukin 6; STAT3, signal transducer and activator of transcription 3.

Article Snippet: Rabbit anti-phospho Stat3 (Ser727) IgG, anti-total STAT3 IgG, anti-phospho ERK1/2 IgG, anti-total ERK1/2 IgG, β-actin and secondary antibody were purchased from Cell Signaling Technology.

Techniques: Activation Assay, Stable Transfection, Expressing, Luciferase, Activity Assay, Control, MTT Assay

Journal: Biomedical Reports

Article Title: Ethyl acetate fraction of Curcuma longa leaves suppresses IL-6-induced STAT3 activation via ERK signaling in Hep3B cells

doi: 10.3892/br.2026.2108

Figure Lengend Snippet: CL-E inhibits IL-6-induced STAT3 phosphorylation and nuclear translocation in Hep3B cells. (A) Hep3B cells were treated with IL-6 (10 ng/ml) for the indicated time periods (0-60 min). Total cell lysates were analyzed by western blotting using antibodies against P-STAT3 (Tyr705), P-STAT3 (Ser727) and total STAT3. (B) Cells were pretreated with the CL-E at 10, 30 and 60 µg/ml for 1 h and then stimulated with IL-6 (10 ng/ml) for 30 min. Proteins were extracted and analyzed by western blotting as described above. (C) STAT3 nuclear translocation was assessed by immunofluorescence microscopy. Hep3B cells were cultured on Nunc Lab-Tek II 8-well chamber slides and treated with IL-6 (10 ng/ml) for 4 h in the absence or presence of CL-E (60 µg/ml) or genistein (60 µM, positive control). Cells were fixed, permeabilized and stained with anti-STAT3 antibody followed by FITC-conjugated secondary antibody. Subcellular localization of STAT3 was visualized using fluorescence microscopy (Scale bar: 20 µm). CL-E, Curcuma longa L. extract; IL-6, interleukin 6; STAT3, signal transducer and activator of transcription 3; P-, phosphorylated.

Techniques: Phospho-proteomics, Translocation Assay, Western Blot, Immunofluorescence, Microscopy, Cell Culture, Positive Control, Staining, Fluorescence

Journal: Biomedical Reports

Article Title: Ethyl acetate fraction of Curcuma longa leaves suppresses IL-6-induced STAT3 activation via ERK signaling in Hep3B cells

doi: 10.3892/br.2026.2108

Figure Lengend Snippet: ERK signaling pathway contributes to CL-E-mediated regulation of IL-6-induced STAT3 activation. (A) Hep3B cells were stimulated with IL-6 (10 ng/ml) for the indicated times (0, 5, 10, 30 and 60 min). Protein lysates underwent western blotting analysis using antibodies against P-ERK1/2 and total ERK1/2 to evaluate time-dependent ERK1/2 activation. (B) Cells were pretreated with CL-E at 10, 30 and 60 µg/ml for 1 h, followed by IL-6 stimulation (10 ng/ml) for 30 min. ERK1/2 phosphorylation was analyzed by western blotting analysis. (C) To investigate the role of ERK in STAT3 Ser727 phosphorylation, cells were treated with CL-E (60 µg/ml), PKC inhibitor bisindolylmaleimide II (20 µM), and/or the MEK1/2 inhibitor U0126 (20 µM) for 1 h in the absence of IL-6. Phosphorylation of STAT3 (Ser727) and total STAT3 were examined by western blotting analysis. (D) To determine whether ERK activation contributes to regulation of STAT3 Tyr705 phosphorylation, cells were pretreated with CL-E, U0126 and/or bisindolylmaleimide II (20 µM) for 1 h before IL-6 stimulation (10 ng/ml, 30 min). STAT3 Tyr705 phosphorylation was analyzed by western blotting. CL-E, Curcuma longa L. extract; IL-6, interleukin 6; STAT3, signal transducer and activator of transcription 3; P-, phosphorylated.

Techniques: Activation Assay, Western Blot, Phospho-proteomics

(A) Volcano plot of differentially secreted proteins from primary LSECs treated with 40 ng/mL LIF versus control (n = 4). (B&C) qPCR of lifr (B) and hgf (C) levels in LSECs isolated from lifr f/f mice with indicated treatments. (D) HGF concentrations in conditioned medium from LSECs treated with hLIF at the indicated doses. (E) HGF concentrations in conditioned medium from LSECs treated with 40 ng/mL hLIF in the presence of the STAT3 inhibitor C188-9 at the indicated doses. (F) HGF concentrations in conditioned medium from LSECs isolated from lifr f/f or lifrΔEC mice treated with hLIF, hCT-1 or hOSM. (G) Western blot analysis of hepatocytes co-cultured with LSECs with or without 40 ng/mL LIF. Quantification is shown in Figure S4C. (H) Model depicting LIF action on LSECs to stimulate angiogenesis and HGF release, thereby supporting hepatocyte proliferation via paracrine regulation.

Journal: bioRxiv

Article Title: The LIF-LIFR Axis Promotes Liver Regeneration via Modulation of Angiogenesis and HGF Release from LSECs

doi: 10.64898/2026.02.24.707802

Figure Lengend Snippet: (A) Volcano plot of differentially secreted proteins from primary LSECs treated with 40 ng/mL LIF versus control (n = 4). (B&C) qPCR of lifr (B) and hgf (C) levels in LSECs isolated from lifr f/f mice with indicated treatments. (D) HGF concentrations in conditioned medium from LSECs treated with hLIF at the indicated doses. (E) HGF concentrations in conditioned medium from LSECs treated with 40 ng/mL hLIF in the presence of the STAT3 inhibitor C188-9 at the indicated doses. (F) HGF concentrations in conditioned medium from LSECs isolated from lifr f/f or lifrΔEC mice treated with hLIF, hCT-1 or hOSM. (G) Western blot analysis of hepatocytes co-cultured with LSECs with or without 40 ng/mL LIF. Quantification is shown in Figure S4C. (H) Model depicting LIF action on LSECs to stimulate angiogenesis and HGF release, thereby supporting hepatocyte proliferation via paracrine regulation.

Article Snippet: The following primary antibodies were used in this study : LIFR (Proteintech, 22779-1-AP, 1:1,000 dilution), Tubulin (Proteintech, 66031-1-Ig, 1:2,000 dilution), Actin (Proteintech, 66009-1-Ig, 1:10,000 dilution), PCNA (Abcam, AB220208, 1:2,000 dilution), p-Y1175-VEGFR2 (Cell Signaling Technology, 3770S, 1:2000 dilution), Total-VEGFR2 (Cell Signaling Technology, 2479S, 1:2000 dilution), p-T705-STAT3 (Cell Signaling Technology, 9145S, 1:2000 dilution), Total-STAT3 (Cell Signaling Technology, 30835S, 1:2,000 dilution), p-T202/Y204-ERK (Cell Signaling Technology, 4370, 1:2,000 dilution) and Total-ERK (Cell Signaling Technology, 4695, 1:2,000 dilution), p-S473-AKT (Cell Signaling Technology, 4060, 1:2,000 dilution), Total-AKT (Cell Signaling Technology, 2920, 1:2000 dilution)

Techniques: Control, Isolation, Western Blot, Cell Culture

( a ) Isolation and characterization of UMSC-EVs. ( b ) Isolation and characterization of EMSC-EVs. ( c ) Characterization of UMSC-EVs and EMSC-EVs by WB. ( d ) AA mouse model. ( e ) H&E staining of skin from AA mice. ( f ) H&E staining of skin from healthy mice. ( g ) Hair growth in each group on day 15. ( h ) Tracing results of EMSC-EVs (green fluorescence). ( i ) Venn diagram. ( j ) Volcano plot. k . Bubble plot of pathway enrichment analysis. l . miR-665 expression in UMSC-EVs and EMSC-EVs. m . Preliminary screening of miRNAs. n . Target prediction of miR-665 via miRDB database. o . Mechanism of miR-665 targeting STAT3 mRNA. p . The results of the dual-luciferase reporter assay. ( n = 3 per group; ns = not significant, *** P < 0.001, **** P < 0.0001)

Journal: Journal of Nanobiotechnology

Article Title: ROS-responsive hydrogel-delivered miR-665 targets STAT3 to alleviate inflammation and promote hair follicle regeneration in alopecia areata

doi: 10.1186/s12951-026-04214-7

Figure Lengend Snippet: ( a ) Isolation and characterization of UMSC-EVs. ( b ) Isolation and characterization of EMSC-EVs. ( c ) Characterization of UMSC-EVs and EMSC-EVs by WB. ( d ) AA mouse model. ( e ) H&E staining of skin from AA mice. ( f ) H&E staining of skin from healthy mice. ( g ) Hair growth in each group on day 15. ( h ) Tracing results of EMSC-EVs (green fluorescence). ( i ) Venn diagram. ( j ) Volcano plot. k . Bubble plot of pathway enrichment analysis. l . miR-665 expression in UMSC-EVs and EMSC-EVs. m . Preliminary screening of miRNAs. n . Target prediction of miR-665 via miRDB database. o . Mechanism of miR-665 targeting STAT3 mRNA. p . The results of the dual-luciferase reporter assay. ( n = 3 per group; ns = not significant, *** P < 0.001, **** P < 0.0001)

Article Snippet: After transfer to polyvinylidene difluoride membranes, rabbit antibodies against phosphorylated STAT3 ( p -STAT3) (1∶2000, CST), mouse antibody against stat3 (1∶2000, CST), mouse antibody against β-actin (1∶1000, Beyotime), and mouse antibody against STAT3 (1∶1000, Beyotime) were used.

Techniques: Isolation, Staining, Fluorescence, Expressing, Luciferase, Reporter Assay

( a ) STAT3 expression in lentivirus-transfected HaCaT cells and DPCs. ( b ) STAT3 expression in lentivirus-transfected HaCaT cells and DPCs before and after IFN-γ treatment. ( c ) STAT3 expression in IFN-γ-treated HaCaT cells and DPCs. ( d ) WB results showing STAT3 expression in lentivirus-transfected HaCaT cells before and after IFN-γ treatment. ( e ) WB results showing STAT3 expression in lentivirus-transfected DPCs before and after IFN-γ treatment. ( f ) Scratch assay results of HaCaT cells. ( g ) 48 h Transwell assay results of DPCs. ( h ) WB results of rescue experiments in HaCaT cells and DPCs. ( i ) Growth of hair follicles in ex vivo culture on day 5 under different treatment conditions. ( n = 3–6 per group; * P < 0.05, ** P < 0.01, *** P < 0.001)

Journal: Journal of Nanobiotechnology

Article Title: ROS-responsive hydrogel-delivered miR-665 targets STAT3 to alleviate inflammation and promote hair follicle regeneration in alopecia areata

doi: 10.1186/s12951-026-04214-7

Figure Lengend Snippet: ( a ) STAT3 expression in lentivirus-transfected HaCaT cells and DPCs. ( b ) STAT3 expression in lentivirus-transfected HaCaT cells and DPCs before and after IFN-γ treatment. ( c ) STAT3 expression in IFN-γ-treated HaCaT cells and DPCs. ( d ) WB results showing STAT3 expression in lentivirus-transfected HaCaT cells before and after IFN-γ treatment. ( e ) WB results showing STAT3 expression in lentivirus-transfected DPCs before and after IFN-γ treatment. ( f ) Scratch assay results of HaCaT cells. ( g ) 48 h Transwell assay results of DPCs. ( h ) WB results of rescue experiments in HaCaT cells and DPCs. ( i ) Growth of hair follicles in ex vivo culture on day 5 under different treatment conditions. ( n = 3–6 per group; * P < 0.05, ** P < 0.01, *** P < 0.001)

Techniques: Expressing, Transfection, Wound Healing Assay, Transwell Assay, Ex Vivo

p-STAT3, phosphorylated STAT3; t-STAT3, total STAT3; ns, non-significant; MFI, mean fluorescence intensity.

Journal: Immune Network

Article Title: IL-22 Exacerbates Coxsackievirus Type B3-Induced Pancreatitis by Elevating Viral Replication Through STAT3 Activation

doi: 10.4110/in.2025.25.e34

Figure Lengend Snippet: p-STAT3, phosphorylated STAT3; t-STAT3, total STAT3; ns, non-significant; MFI, mean fluorescence intensity.

Article Snippet: Rabbit anti-total STAT3 (Cell Signaling Technology), rabbit anti-phosphorylated STAT3 (Cell Signaling Technology), and rat anti-Mouse IL-22ra1 (R&D system) Abs were diluted to 1:1,000.

Techniques: Fluorescence

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