Review



stat3 inhibitor stattic  (MedChemExpress)


Bioz Verified Symbol MedChemExpress is a verified supplier
Bioz Manufacturer Symbol MedChemExpress manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 99
      Buy from Supplier

    Structured Review

    MedChemExpress stat3 inhibitor stattic
    S100A8/A9 hi macrophages mediate CCL6 expression through activation of the transcription factor <t>STAT3.</t> (A) Venn diagram integrating multiple bioinformatic databases to identify potential upstream transcription factors regulating Ccl6 expression. (B) Protein‐protein interaction network between the nine transcription factors and S100A9. (C–F) BMDMs were stimulated with recombinant S100A8‐S100A9 protein (1 µg/mL) with or without pretreated with FPS‐ZM1 (1 µ m ), TAK‐242 (1 µ m ) or DMSO vehicle for 1 h. p‐STAT3 and total STAT3 were assessed by Western blot at 2 h (C and D), and CCL6 levels in culture supernatants were measured by ELISA at 24 h (E). The colocalization of S100A8/A9 with TLR4 in BMDMs was assessed by immunofluorescence staining (F); Scale bar, 20 µm. (G,H) Following pretreatment with or without Stattic (5 µ m ) for 1 h, BMDMs were stimulated with recombinant S100A8‐S100A9 protein (1 µg/mL). p‐STAT3 and total STAT3 levels were assessed by Western blot at 2 h (G), and CCL6 in culture supernatants was quantified by ELISA at 24 h (H). (I,J) BMDMs were transfected with siNC or si S100a9 , followed by treatment with Colivelin TFA (50 µg/mL) for 4 h to activate STAT3. Protein levels of S100A9, p‐STAT3/STAT3, and CCL6 were measured by Western blot (I), and p‐STAT3 expression was visualized by immunofluorescence (J; Scale bar: 500 µm). (K) Western blot analysis of p‐STAT3 levels in nuclear and cytoplasmic fractions of BMDMs transfected with siNC or siS100a9 . (L) Schematic representation of putative STAT3 binding sites within the Ccl6 promoter. (M) Dual‐luciferase reporter assays were performed in HEK 293T cells co‐transfected with a control vector (NC) or a Stat3 expression plasmid, together with reporter vectors pGL1‐Control, pGL1‐Ccl6 wild‐type (WT), or pGL1‐Ccl6 mutant (mut). Promoter activity was measured and normalized. N, O) BMDMs were treated with recombinant S100A8‐S100A9 protein (1 µg/mL) for 2 h. STAT3 recruitment to the Ccl6 promoter was analyzed by chromatin immunoprecipitation (ChIP) assay. The enrichment of p‐STAT3 at the promoter region was quantified by RT‐qPCR and expressed as a percentage of the total input (N). Representative agarose gel images confirmed the specificity of the PCR amplification (O). All values are expressed as mean ± SD. ns, no significant difference, * p < 0.05, ** p < 0.01, *** p < 0.001.
    Stat3 Inhibitor Stattic, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 434 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/stat3+inhibitor+stattic/Stattic/pmc13336410-222-71-77
    Average 99 stars, based on 434 article reviews
    stat3 inhibitor stattic - by Bioz Stars, 2026-10
    99/100 stars

    Images

    1) Product Images from "S100A8/A9‐High Macrophages Activate Intestinal Fibroblasts via mCCL6/hCCL15‐CCR1 Axis to Drive Intestinal Fibrosis in Crohn's Disease"

    Article Title: S100A8/A9‐High Macrophages Activate Intestinal Fibroblasts via mCCL6/hCCL15‐CCR1 Axis to Drive Intestinal Fibrosis in Crohn's Disease

    Journal: Advanced Science

    doi: 10.1002/advs.76353

    S100A8/A9 hi macrophages mediate CCL6 expression through activation of the transcription factor STAT3. (A) Venn diagram integrating multiple bioinformatic databases to identify potential upstream transcription factors regulating Ccl6 expression. (B) Protein‐protein interaction network between the nine transcription factors and S100A9. (C–F) BMDMs were stimulated with recombinant S100A8‐S100A9 protein (1 µg/mL) with or without pretreated with FPS‐ZM1 (1 µ m ), TAK‐242 (1 µ m ) or DMSO vehicle for 1 h. p‐STAT3 and total STAT3 were assessed by Western blot at 2 h (C and D), and CCL6 levels in culture supernatants were measured by ELISA at 24 h (E). The colocalization of S100A8/A9 with TLR4 in BMDMs was assessed by immunofluorescence staining (F); Scale bar, 20 µm. (G,H) Following pretreatment with or without Stattic (5 µ m ) for 1 h, BMDMs were stimulated with recombinant S100A8‐S100A9 protein (1 µg/mL). p‐STAT3 and total STAT3 levels were assessed by Western blot at 2 h (G), and CCL6 in culture supernatants was quantified by ELISA at 24 h (H). (I,J) BMDMs were transfected with siNC or si S100a9 , followed by treatment with Colivelin TFA (50 µg/mL) for 4 h to activate STAT3. Protein levels of S100A9, p‐STAT3/STAT3, and CCL6 were measured by Western blot (I), and p‐STAT3 expression was visualized by immunofluorescence (J; Scale bar: 500 µm). (K) Western blot analysis of p‐STAT3 levels in nuclear and cytoplasmic fractions of BMDMs transfected with siNC or siS100a9 . (L) Schematic representation of putative STAT3 binding sites within the Ccl6 promoter. (M) Dual‐luciferase reporter assays were performed in HEK 293T cells co‐transfected with a control vector (NC) or a Stat3 expression plasmid, together with reporter vectors pGL1‐Control, pGL1‐Ccl6 wild‐type (WT), or pGL1‐Ccl6 mutant (mut). Promoter activity was measured and normalized. N, O) BMDMs were treated with recombinant S100A8‐S100A9 protein (1 µg/mL) for 2 h. STAT3 recruitment to the Ccl6 promoter was analyzed by chromatin immunoprecipitation (ChIP) assay. The enrichment of p‐STAT3 at the promoter region was quantified by RT‐qPCR and expressed as a percentage of the total input (N). Representative agarose gel images confirmed the specificity of the PCR amplification (O). All values are expressed as mean ± SD. ns, no significant difference, * p < 0.05, ** p < 0.01, *** p < 0.001.
    Figure Legend Snippet: S100A8/A9 hi macrophages mediate CCL6 expression through activation of the transcription factor STAT3. (A) Venn diagram integrating multiple bioinformatic databases to identify potential upstream transcription factors regulating Ccl6 expression. (B) Protein‐protein interaction network between the nine transcription factors and S100A9. (C–F) BMDMs were stimulated with recombinant S100A8‐S100A9 protein (1 µg/mL) with or without pretreated with FPS‐ZM1 (1 µ m ), TAK‐242 (1 µ m ) or DMSO vehicle for 1 h. p‐STAT3 and total STAT3 were assessed by Western blot at 2 h (C and D), and CCL6 levels in culture supernatants were measured by ELISA at 24 h (E). The colocalization of S100A8/A9 with TLR4 in BMDMs was assessed by immunofluorescence staining (F); Scale bar, 20 µm. (G,H) Following pretreatment with or without Stattic (5 µ m ) for 1 h, BMDMs were stimulated with recombinant S100A8‐S100A9 protein (1 µg/mL). p‐STAT3 and total STAT3 levels were assessed by Western blot at 2 h (G), and CCL6 in culture supernatants was quantified by ELISA at 24 h (H). (I,J) BMDMs were transfected with siNC or si S100a9 , followed by treatment with Colivelin TFA (50 µg/mL) for 4 h to activate STAT3. Protein levels of S100A9, p‐STAT3/STAT3, and CCL6 were measured by Western blot (I), and p‐STAT3 expression was visualized by immunofluorescence (J; Scale bar: 500 µm). (K) Western blot analysis of p‐STAT3 levels in nuclear and cytoplasmic fractions of BMDMs transfected with siNC or siS100a9 . (L) Schematic representation of putative STAT3 binding sites within the Ccl6 promoter. (M) Dual‐luciferase reporter assays were performed in HEK 293T cells co‐transfected with a control vector (NC) or a Stat3 expression plasmid, together with reporter vectors pGL1‐Control, pGL1‐Ccl6 wild‐type (WT), or pGL1‐Ccl6 mutant (mut). Promoter activity was measured and normalized. N, O) BMDMs were treated with recombinant S100A8‐S100A9 protein (1 µg/mL) for 2 h. STAT3 recruitment to the Ccl6 promoter was analyzed by chromatin immunoprecipitation (ChIP) assay. The enrichment of p‐STAT3 at the promoter region was quantified by RT‐qPCR and expressed as a percentage of the total input (N). Representative agarose gel images confirmed the specificity of the PCR amplification (O). All values are expressed as mean ± SD. ns, no significant difference, * p < 0.05, ** p < 0.01, *** p < 0.001.

    Techniques Used: Expressing, Activation Assay, Recombinant, Western Blot, Enzyme-linked Immunosorbent Assay, Immunofluorescence, Staining, Transfection, Binding Assay, Luciferase, Control, Plasmid Preparation, Mutagenesis, Activity Assay, Chromatin Immunoprecipitation, Quantitative RT-PCR, Agarose Gel Electrophoresis, Amplification

    Related Articles

    Recombinant:

    Article Title: S100A8/A9‐High Macrophages Activate Intestinal Fibroblasts via mCCL6/hCCL15‐CCR1 Axis to Drive Intestinal Fibrosis in Crohn's Disease
    Article Snippet: To evaluate the profibrotic effects of S100A8/A9 hi BMDM‐derived CCL6, two strategies were used: (1) BMDMs were pre‐incubated for 6 h with an anti‐CCL6 antibody (40 ng/mL; R&D Systems, MAB487) or an IgG2B isotype control (40 ng/mL; R&D Systems, MAB0061); (2) NIH‐3T3 cells were pretreated for 6 h with the CCR1 inhibitor BX471 (20 μM) or DMSO vehicle control (0.05%) prior to co‐culture. .. To investigate the role of the STAT3 pathway in S100A8/A9‐mediated CCL6 production, BMDMs were stimulated with recombinant S100A8‐S100A9 heterodimer (1 μg/mL; HY‐P71076; MCE, USA) for 2 h. To identify the functional receptors mediating S100A8/A9‐induced STAT3 activation, BMDMs were pretreated with the TLR4 inhibitor TAK‐242 (1 μM; HY‐11109; MCE, USA) or the RAGE inhibitor FPS‐ZM1 (1 μM; HY‐19370; MCE, USA) for 1 h. For STAT3 pathway blockade, BMDMs were pretreated with the STAT3 inhibitor Stattic (5 μM; HY‐13818; MCE, USA) for 1 h before stimulation. .. For rescue experiments, BMDMs were transfected with siRNA targeting S100a9, followed by treatment with or without the STAT3 activator Colivelin TFA (50 μg/mL; HY‐P1061A; MCE, USA), which was added to the culture medium 4 h prior to downstream analysis.

    Functional Assay:

    Article Title: S100A8/A9‐High Macrophages Activate Intestinal Fibroblasts via mCCL6/hCCL15‐CCR1 Axis to Drive Intestinal Fibrosis in Crohn's Disease
    Article Snippet: To evaluate the profibrotic effects of S100A8/A9 hi BMDM‐derived CCL6, two strategies were used: (1) BMDMs were pre‐incubated for 6 h with an anti‐CCL6 antibody (40 ng/mL; R&D Systems, MAB487) or an IgG2B isotype control (40 ng/mL; R&D Systems, MAB0061); (2) NIH‐3T3 cells were pretreated for 6 h with the CCR1 inhibitor BX471 (20 μM) or DMSO vehicle control (0.05%) prior to co‐culture. .. To investigate the role of the STAT3 pathway in S100A8/A9‐mediated CCL6 production, BMDMs were stimulated with recombinant S100A8‐S100A9 heterodimer (1 μg/mL; HY‐P71076; MCE, USA) for 2 h. To identify the functional receptors mediating S100A8/A9‐induced STAT3 activation, BMDMs were pretreated with the TLR4 inhibitor TAK‐242 (1 μM; HY‐11109; MCE, USA) or the RAGE inhibitor FPS‐ZM1 (1 μM; HY‐19370; MCE, USA) for 1 h. For STAT3 pathway blockade, BMDMs were pretreated with the STAT3 inhibitor Stattic (5 μM; HY‐13818; MCE, USA) for 1 h before stimulation. .. For rescue experiments, BMDMs were transfected with siRNA targeting S100a9, followed by treatment with or without the STAT3 activator Colivelin TFA (50 μg/mL; HY‐P1061A; MCE, USA), which was added to the culture medium 4 h prior to downstream analysis.

    Activation Assay:

    Article Title: S100A8/A9‐High Macrophages Activate Intestinal Fibroblasts via mCCL6/hCCL15‐CCR1 Axis to Drive Intestinal Fibrosis in Crohn's Disease
    Article Snippet: To evaluate the profibrotic effects of S100A8/A9 hi BMDM‐derived CCL6, two strategies were used: (1) BMDMs were pre‐incubated for 6 h with an anti‐CCL6 antibody (40 ng/mL; R&D Systems, MAB487) or an IgG2B isotype control (40 ng/mL; R&D Systems, MAB0061); (2) NIH‐3T3 cells were pretreated for 6 h with the CCR1 inhibitor BX471 (20 μM) or DMSO vehicle control (0.05%) prior to co‐culture. .. To investigate the role of the STAT3 pathway in S100A8/A9‐mediated CCL6 production, BMDMs were stimulated with recombinant S100A8‐S100A9 heterodimer (1 μg/mL; HY‐P71076; MCE, USA) for 2 h. To identify the functional receptors mediating S100A8/A9‐induced STAT3 activation, BMDMs were pretreated with the TLR4 inhibitor TAK‐242 (1 μM; HY‐11109; MCE, USA) or the RAGE inhibitor FPS‐ZM1 (1 μM; HY‐19370; MCE, USA) for 1 h. For STAT3 pathway blockade, BMDMs were pretreated with the STAT3 inhibitor Stattic (5 μM; HY‐13818; MCE, USA) for 1 h before stimulation. .. For rescue experiments, BMDMs were transfected with siRNA targeting S100a9, followed by treatment with or without the STAT3 activator Colivelin TFA (50 μg/mL; HY‐P1061A; MCE, USA), which was added to the culture medium 4 h prior to downstream analysis.

    other:

    Article Title: PEAK1 promotes prostate cancer progression and docetaxel resistance by mediating the polarization of tumor-associated macrophages
    Article Snippet: The PC3 and DU145 cells were treated with the HIF-1α inhibitor LW6 (10 μM, #HY-13671, MedChemExpress) [ ]; the STAT3 inhibitor Stattic (10 μM, #HY-13818, MedChemExpress) [ ]; the NF-κB inhibitor Bay 11–7082 (15 μM, #HY-13453, MedChemExpress) [ ]; and increasing doses of enzalutamide (5 μM, 10 μM, 20 μM, and 40 μM, #HY-70002, MedChemExpress) [ ] for 24 h.



    Similar Products

    stat3 inhibitor stattic  (MedChemExpress)
    99
    MedChemExpress stat3 inhibitor stattic
    S100A8/A9 hi macrophages mediate CCL6 expression through activation of the transcription factor <t>STAT3.</t> (A) Venn diagram integrating multiple bioinformatic databases to identify potential upstream transcription factors regulating Ccl6 expression. (B) Protein‐protein interaction network between the nine transcription factors and S100A9. (C–F) BMDMs were stimulated with recombinant S100A8‐S100A9 protein (1 µg/mL) with or without pretreated with FPS‐ZM1 (1 µ m ), TAK‐242 (1 µ m ) or DMSO vehicle for 1 h. p‐STAT3 and total STAT3 were assessed by Western blot at 2 h (C and D), and CCL6 levels in culture supernatants were measured by ELISA at 24 h (E). The colocalization of S100A8/A9 with TLR4 in BMDMs was assessed by immunofluorescence staining (F); Scale bar, 20 µm. (G,H) Following pretreatment with or without Stattic (5 µ m ) for 1 h, BMDMs were stimulated with recombinant S100A8‐S100A9 protein (1 µg/mL). p‐STAT3 and total STAT3 levels were assessed by Western blot at 2 h (G), and CCL6 in culture supernatants was quantified by ELISA at 24 h (H). (I,J) BMDMs were transfected with siNC or si S100a9 , followed by treatment with Colivelin TFA (50 µg/mL) for 4 h to activate STAT3. Protein levels of S100A9, p‐STAT3/STAT3, and CCL6 were measured by Western blot (I), and p‐STAT3 expression was visualized by immunofluorescence (J; Scale bar: 500 µm). (K) Western blot analysis of p‐STAT3 levels in nuclear and cytoplasmic fractions of BMDMs transfected with siNC or siS100a9 . (L) Schematic representation of putative STAT3 binding sites within the Ccl6 promoter. (M) Dual‐luciferase reporter assays were performed in HEK 293T cells co‐transfected with a control vector (NC) or a Stat3 expression plasmid, together with reporter vectors pGL1‐Control, pGL1‐Ccl6 wild‐type (WT), or pGL1‐Ccl6 mutant (mut). Promoter activity was measured and normalized. N, O) BMDMs were treated with recombinant S100A8‐S100A9 protein (1 µg/mL) for 2 h. STAT3 recruitment to the Ccl6 promoter was analyzed by chromatin immunoprecipitation (ChIP) assay. The enrichment of p‐STAT3 at the promoter region was quantified by RT‐qPCR and expressed as a percentage of the total input (N). Representative agarose gel images confirmed the specificity of the PCR amplification (O). All values are expressed as mean ± SD. ns, no significant difference, * p < 0.05, ** p < 0.01, *** p < 0.001.
    Stat3 Inhibitor Stattic, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/stat3+inhibitor+stattic/Stattic/pmc13336410-222-71-77
    Average 99 stars, based on 1 article reviews
    stat3 inhibitor stattic - by Bioz Stars, 2026-10
    99/100 stars
    		  Buy from Supplier
    stat3 inhibitor  (MedChemExpress)
    99
    MedChemExpress stat3 inhibitor
    S100A8/A9 hi macrophages mediate CCL6 expression through activation of the transcription factor <t>STAT3.</t> (A) Venn diagram integrating multiple bioinformatic databases to identify potential upstream transcription factors regulating Ccl6 expression. (B) Protein‐protein interaction network between the nine transcription factors and S100A9. (C–F) BMDMs were stimulated with recombinant S100A8‐S100A9 protein (1 µg/mL) with or without pretreated with FPS‐ZM1 (1 µ m ), TAK‐242 (1 µ m ) or DMSO vehicle for 1 h. p‐STAT3 and total STAT3 were assessed by Western blot at 2 h (C and D), and CCL6 levels in culture supernatants were measured by ELISA at 24 h (E). The colocalization of S100A8/A9 with TLR4 in BMDMs was assessed by immunofluorescence staining (F); Scale bar, 20 µm. (G,H) Following pretreatment with or without Stattic (5 µ m ) for 1 h, BMDMs were stimulated with recombinant S100A8‐S100A9 protein (1 µg/mL). p‐STAT3 and total STAT3 levels were assessed by Western blot at 2 h (G), and CCL6 in culture supernatants was quantified by ELISA at 24 h (H). (I,J) BMDMs were transfected with siNC or si S100a9 , followed by treatment with Colivelin TFA (50 µg/mL) for 4 h to activate STAT3. Protein levels of S100A9, p‐STAT3/STAT3, and CCL6 were measured by Western blot (I), and p‐STAT3 expression was visualized by immunofluorescence (J; Scale bar: 500 µm). (K) Western blot analysis of p‐STAT3 levels in nuclear and cytoplasmic fractions of BMDMs transfected with siNC or siS100a9 . (L) Schematic representation of putative STAT3 binding sites within the Ccl6 promoter. (M) Dual‐luciferase reporter assays were performed in HEK 293T cells co‐transfected with a control vector (NC) or a Stat3 expression plasmid, together with reporter vectors pGL1‐Control, pGL1‐Ccl6 wild‐type (WT), or pGL1‐Ccl6 mutant (mut). Promoter activity was measured and normalized. N, O) BMDMs were treated with recombinant S100A8‐S100A9 protein (1 µg/mL) for 2 h. STAT3 recruitment to the Ccl6 promoter was analyzed by chromatin immunoprecipitation (ChIP) assay. The enrichment of p‐STAT3 at the promoter region was quantified by RT‐qPCR and expressed as a percentage of the total input (N). Representative agarose gel images confirmed the specificity of the PCR amplification (O). All values are expressed as mean ± SD. ns, no significant difference, * p < 0.05, ** p < 0.01, *** p < 0.001.
    Stat3 Inhibitor, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/stat3+inhibitor+stattic/Stattic/pmc13230207-101-38-41
    Average 99 stars, based on 1 article reviews
    stat3 inhibitor - by Bioz Stars, 2026-10
    99/100 stars
    		  Buy from Supplier
    stat3 specific inhibitor stattic  (MedChemExpress)
    99
    MedChemExpress stat3 specific inhibitor stattic
    Proposed pathophysiological framework of ovariectomy (OVX)-induced osteoporosis and the protective effects of valproic acid (VPA). (Top) OVX disrupts bone homoeostasis, characterised by sustained osteoclast overactivation and compromised osteoblast survival. Concurrently, the accumulation of M1-polarised macrophages is associated with inflammatory infiltration, contributing to exacerbated bone loss. (Bottom) The M1 macrophage secretome, enriched in pro-inflammatory cytokines (e.g. IL-6), creates a microenvironment that supports osteoclastogenesis and contributes to ferroptosis in osteoblasts. VPA counteracts these pathological shifts by targeting HIF-1α to restrict glycolysis-driven M1 polarisation in macrophages. This attenuation of M1 polarisation correlates with reduced IL-6 secretion and the subsequent downregulation of the p <t>-STAT3/HIF-1α/TFRC</t> signalling axis, ultimately alleviating iron overload-associated oxidative stress.
    Stat3 Specific Inhibitor Stattic, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/stat3+inhibitor+stattic/Stattic/pmc13137742-48-28-34
    Average 99 stars, based on 1 article reviews
    stat3 specific inhibitor stattic - by Bioz Stars, 2026-10
    99/100 stars
    		  Buy from Supplier
    transcription 3 stat3 phosphorylation inhibitor stattic  (MedChemExpress)
    99
    MedChemExpress transcription 3 stat3 phosphorylation inhibitor stattic
    CKAP2L promotes proliferation and migration of colorectal cancer cells through the <t>STAT3/AREG/EGFR</t> axis. (A) Expression levels of STAT3 and p-STAT3 proteins measured by western blotting. (B) Calculation of IC 50 in HCT116 cells treated with Stattic for 24 h. (C) Levels of AREG were measured by reverse transcription-quantitative PCR and enzyme-linked immunosorbent assay. (D) Migration of cells was detected by Transwell assay (×100 magnification). (E) Proliferation of cells was measured by Cell Counting Kit 8. (F) Expression levels of proteins measured by western blotting. (G) Binding peak of STAT3 on the promoter region of AREG was detected by Cistrome Data Browser, the binding motif was predicted using the JASPAR database, and the binding of STAT3 to the AREG promoter was evaluated by chromatin immunoprecipitation assay. Data were analyzed using (A and G) Unpaired Student's t-test, and (C-F) two-way ANOVA followed by Tukey test. * P<0.05, ** P<0.01, *** P<0.001 and **** P<0.0001. AREG, amphiregulin; CKAP2L, cytoskeleton-associated protein 2-like; EGFR, epidermal growth factor receptor; NC, negative control; p-, phosphorylated; sh, short hairpin; STAT3, signal transducer and activator of transcription 3; TSS, transcription start site.
    Transcription 3 Stat3 Phosphorylation Inhibitor Stattic, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/stat3+inhibitor+stattic/Stattic/pmc13038336-98-6-15
    Average 99 stars, based on 1 article reviews
    transcription 3 stat3 phosphorylation inhibitor stattic - by Bioz Stars, 2026-10
    99/100 stars
    		  Buy from Supplier
    stat3 inhibitor stattic  (Selleck Chemicals)
    96
    Selleck Chemicals stat3 inhibitor stattic
    CKAP2L promotes proliferation and migration of colorectal cancer cells through the <t>STAT3/AREG/EGFR</t> axis. (A) Expression levels of STAT3 and p-STAT3 proteins measured by western blotting. (B) Calculation of IC 50 in HCT116 cells treated with Stattic for 24 h. (C) Levels of AREG were measured by reverse transcription-quantitative PCR and enzyme-linked immunosorbent assay. (D) Migration of cells was detected by Transwell assay (×100 magnification). (E) Proliferation of cells was measured by Cell Counting Kit 8. (F) Expression levels of proteins measured by western blotting. (G) Binding peak of STAT3 on the promoter region of AREG was detected by Cistrome Data Browser, the binding motif was predicted using the JASPAR database, and the binding of STAT3 to the AREG promoter was evaluated by chromatin immunoprecipitation assay. Data were analyzed using (A and G) Unpaired Student's t-test, and (C-F) two-way ANOVA followed by Tukey test. * P<0.05, ** P<0.01, *** P<0.001 and **** P<0.0001. AREG, amphiregulin; CKAP2L, cytoskeleton-associated protein 2-like; EGFR, epidermal growth factor receptor; NC, negative control; p-, phosphorylated; sh, short hairpin; STAT3, signal transducer and activator of transcription 3; TSS, transcription start site.
    Stat3 Inhibitor Stattic, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/stat3+inhibitor+stattic/Stattic/pm41871146-95-10-17
    Average 96 stars, based on 1 article reviews
    stat3 inhibitor stattic - by Bioz Stars, 2026-10
    96/100 stars
    		  Buy from Supplier
    stat3 phosphorylation inhibitor stattic  (MedChemExpress)
    99
    MedChemExpress stat3 phosphorylation inhibitor stattic
    CKAP2L promotes proliferation and migration of colorectal cancer cells through the <t>STAT3/AREG/EGFR</t> axis. (A) Expression levels of STAT3 and p-STAT3 proteins measured by western blotting. (B) Calculation of IC 50 in HCT116 cells treated with Stattic for 24 h. (C) Levels of AREG were measured by reverse transcription-quantitative PCR and enzyme-linked immunosorbent assay. (D) Migration of cells was detected by Transwell assay (×100 magnification). (E) Proliferation of cells was measured by Cell Counting Kit 8. (F) Expression levels of proteins measured by western blotting. (G) Binding peak of STAT3 on the promoter region of AREG was detected by Cistrome Data Browser, the binding motif was predicted using the JASPAR database, and the binding of STAT3 to the AREG promoter was evaluated by chromatin immunoprecipitation assay. Data were analyzed using (A and G) Unpaired Student's t-test, and (C-F) two-way ANOVA followed by Tukey test. * P<0.05, ** P<0.01, *** P<0.001 and **** P<0.0001. AREG, amphiregulin; CKAP2L, cytoskeleton-associated protein 2-like; EGFR, epidermal growth factor receptor; NC, negative control; p-, phosphorylated; sh, short hairpin; STAT3, signal transducer and activator of transcription 3; TSS, transcription start site.
    Stat3 Phosphorylation Inhibitor Stattic, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/stat3+inhibitor+stattic/Stattic/pm41833704-84-32-38
    Average 99 stars, based on 1 article reviews
    stat3 phosphorylation inhibitor stattic - by Bioz Stars, 2026-10
    99/100 stars
    		  Buy from Supplier
    stat3 inhibitor  (Selleck Chemicals)
    96
    Selleck Chemicals stat3 inhibitor
    CKAP2L promotes proliferation and migration of colorectal cancer cells through the <t>STAT3/AREG/EGFR</t> axis. (A) Expression levels of STAT3 and p-STAT3 proteins measured by western blotting. (B) Calculation of IC 50 in HCT116 cells treated with Stattic for 24 h. (C) Levels of AREG were measured by reverse transcription-quantitative PCR and enzyme-linked immunosorbent assay. (D) Migration of cells was detected by Transwell assay (×100 magnification). (E) Proliferation of cells was measured by Cell Counting Kit 8. (F) Expression levels of proteins measured by western blotting. (G) Binding peak of STAT3 on the promoter region of AREG was detected by Cistrome Data Browser, the binding motif was predicted using the JASPAR database, and the binding of STAT3 to the AREG promoter was evaluated by chromatin immunoprecipitation assay. Data were analyzed using (A and G) Unpaired Student's t-test, and (C-F) two-way ANOVA followed by Tukey test. * P<0.05, ** P<0.01, *** P<0.001 and **** P<0.0001. AREG, amphiregulin; CKAP2L, cytoskeleton-associated protein 2-like; EGFR, epidermal growth factor receptor; NC, negative control; p-, phosphorylated; sh, short hairpin; STAT3, signal transducer and activator of transcription 3; TSS, transcription start site.
    Stat3 Inhibitor, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/stat3+inhibitor+stattic/Stattic/pmc12976258-305-45-48
    Average 96 stars, based on 1 article reviews
    stat3 inhibitor - by Bioz Stars, 2026-10
    96/100 stars
    		  Buy from Supplier

    Image Search Results


    S100A8/A9 hi macrophages mediate CCL6 expression through activation of the transcription factor STAT3. (A) Venn diagram integrating multiple bioinformatic databases to identify potential upstream transcription factors regulating Ccl6 expression. (B) Protein‐protein interaction network between the nine transcription factors and S100A9. (C–F) BMDMs were stimulated with recombinant S100A8‐S100A9 protein (1 µg/mL) with or without pretreated with FPS‐ZM1 (1 µ m ), TAK‐242 (1 µ m ) or DMSO vehicle for 1 h. p‐STAT3 and total STAT3 were assessed by Western blot at 2 h (C and D), and CCL6 levels in culture supernatants were measured by ELISA at 24 h (E). The colocalization of S100A8/A9 with TLR4 in BMDMs was assessed by immunofluorescence staining (F); Scale bar, 20 µm. (G,H) Following pretreatment with or without Stattic (5 µ m ) for 1 h, BMDMs were stimulated with recombinant S100A8‐S100A9 protein (1 µg/mL). p‐STAT3 and total STAT3 levels were assessed by Western blot at 2 h (G), and CCL6 in culture supernatants was quantified by ELISA at 24 h (H). (I,J) BMDMs were transfected with siNC or si S100a9 , followed by treatment with Colivelin TFA (50 µg/mL) for 4 h to activate STAT3. Protein levels of S100A9, p‐STAT3/STAT3, and CCL6 were measured by Western blot (I), and p‐STAT3 expression was visualized by immunofluorescence (J; Scale bar: 500 µm). (K) Western blot analysis of p‐STAT3 levels in nuclear and cytoplasmic fractions of BMDMs transfected with siNC or siS100a9 . (L) Schematic representation of putative STAT3 binding sites within the Ccl6 promoter. (M) Dual‐luciferase reporter assays were performed in HEK 293T cells co‐transfected with a control vector (NC) or a Stat3 expression plasmid, together with reporter vectors pGL1‐Control, pGL1‐Ccl6 wild‐type (WT), or pGL1‐Ccl6 mutant (mut). Promoter activity was measured and normalized. N, O) BMDMs were treated with recombinant S100A8‐S100A9 protein (1 µg/mL) for 2 h. STAT3 recruitment to the Ccl6 promoter was analyzed by chromatin immunoprecipitation (ChIP) assay. The enrichment of p‐STAT3 at the promoter region was quantified by RT‐qPCR and expressed as a percentage of the total input (N). Representative agarose gel images confirmed the specificity of the PCR amplification (O). All values are expressed as mean ± SD. ns, no significant difference, * p < 0.05, ** p < 0.01, *** p < 0.001.

    Journal: Advanced Science

    Article Title: S100A8/A9‐High Macrophages Activate Intestinal Fibroblasts via mCCL6/hCCL15‐CCR1 Axis to Drive Intestinal Fibrosis in Crohn's Disease

    doi: 10.1002/advs.76353

    Figure Lengend Snippet: S100A8/A9 hi macrophages mediate CCL6 expression through activation of the transcription factor STAT3. (A) Venn diagram integrating multiple bioinformatic databases to identify potential upstream transcription factors regulating Ccl6 expression. (B) Protein‐protein interaction network between the nine transcription factors and S100A9. (C–F) BMDMs were stimulated with recombinant S100A8‐S100A9 protein (1 µg/mL) with or without pretreated with FPS‐ZM1 (1 µ m ), TAK‐242 (1 µ m ) or DMSO vehicle for 1 h. p‐STAT3 and total STAT3 were assessed by Western blot at 2 h (C and D), and CCL6 levels in culture supernatants were measured by ELISA at 24 h (E). The colocalization of S100A8/A9 with TLR4 in BMDMs was assessed by immunofluorescence staining (F); Scale bar, 20 µm. (G,H) Following pretreatment with or without Stattic (5 µ m ) for 1 h, BMDMs were stimulated with recombinant S100A8‐S100A9 protein (1 µg/mL). p‐STAT3 and total STAT3 levels were assessed by Western blot at 2 h (G), and CCL6 in culture supernatants was quantified by ELISA at 24 h (H). (I,J) BMDMs were transfected with siNC or si S100a9 , followed by treatment with Colivelin TFA (50 µg/mL) for 4 h to activate STAT3. Protein levels of S100A9, p‐STAT3/STAT3, and CCL6 were measured by Western blot (I), and p‐STAT3 expression was visualized by immunofluorescence (J; Scale bar: 500 µm). (K) Western blot analysis of p‐STAT3 levels in nuclear and cytoplasmic fractions of BMDMs transfected with siNC or siS100a9 . (L) Schematic representation of putative STAT3 binding sites within the Ccl6 promoter. (M) Dual‐luciferase reporter assays were performed in HEK 293T cells co‐transfected with a control vector (NC) or a Stat3 expression plasmid, together with reporter vectors pGL1‐Control, pGL1‐Ccl6 wild‐type (WT), or pGL1‐Ccl6 mutant (mut). Promoter activity was measured and normalized. N, O) BMDMs were treated with recombinant S100A8‐S100A9 protein (1 µg/mL) for 2 h. STAT3 recruitment to the Ccl6 promoter was analyzed by chromatin immunoprecipitation (ChIP) assay. The enrichment of p‐STAT3 at the promoter region was quantified by RT‐qPCR and expressed as a percentage of the total input (N). Representative agarose gel images confirmed the specificity of the PCR amplification (O). All values are expressed as mean ± SD. ns, no significant difference, * p < 0.05, ** p < 0.01, *** p < 0.001.

    Article Snippet: To investigate the role of the STAT3 pathway in S100A8/A9‐mediated CCL6 production, BMDMs were stimulated with recombinant S100A8‐S100A9 heterodimer (1 μg/mL; HY‐P71076; MCE, USA) for 2 h. To identify the functional receptors mediating S100A8/A9‐induced STAT3 activation, BMDMs were pretreated with the TLR4 inhibitor TAK‐242 (1 μM; HY‐11109; MCE, USA) or the RAGE inhibitor FPS‐ZM1 (1 μM; HY‐19370; MCE, USA) for 1 h. For STAT3 pathway blockade, BMDMs were pretreated with the STAT3 inhibitor Stattic (5 μM; HY‐13818; MCE, USA) for 1 h before stimulation.

    Techniques: Expressing, Activation Assay, Recombinant, Western Blot, Enzyme-linked Immunosorbent Assay, Immunofluorescence, Staining, Transfection, Binding Assay, Luciferase, Control, Plasmid Preparation, Mutagenesis, Activity Assay, Chromatin Immunoprecipitation, Quantitative RT-PCR, Agarose Gel Electrophoresis, Amplification

    Proposed pathophysiological framework of ovariectomy (OVX)-induced osteoporosis and the protective effects of valproic acid (VPA). (Top) OVX disrupts bone homoeostasis, characterised by sustained osteoclast overactivation and compromised osteoblast survival. Concurrently, the accumulation of M1-polarised macrophages is associated with inflammatory infiltration, contributing to exacerbated bone loss. (Bottom) The M1 macrophage secretome, enriched in pro-inflammatory cytokines (e.g. IL-6), creates a microenvironment that supports osteoclastogenesis and contributes to ferroptosis in osteoblasts. VPA counteracts these pathological shifts by targeting HIF-1α to restrict glycolysis-driven M1 polarisation in macrophages. This attenuation of M1 polarisation correlates with reduced IL-6 secretion and the subsequent downregulation of the p -STAT3/HIF-1α/TFRC signalling axis, ultimately alleviating iron overload-associated oxidative stress.

    Journal: Redox Report : Communications in Free Radical Research

    Article Title: Macrophage metabolic reprogramming via HIF-1α–glycolysis drives osteoblast ferroptosis and bone loss through an IL-6–STAT3–dependent redox axis

    doi: 10.1080/13510002.2026.2667673

    Figure Lengend Snippet: Proposed pathophysiological framework of ovariectomy (OVX)-induced osteoporosis and the protective effects of valproic acid (VPA). (Top) OVX disrupts bone homoeostasis, characterised by sustained osteoclast overactivation and compromised osteoblast survival. Concurrently, the accumulation of M1-polarised macrophages is associated with inflammatory infiltration, contributing to exacerbated bone loss. (Bottom) The M1 macrophage secretome, enriched in pro-inflammatory cytokines (e.g. IL-6), creates a microenvironment that supports osteoclastogenesis and contributes to ferroptosis in osteoblasts. VPA counteracts these pathological shifts by targeting HIF-1α to restrict glycolysis-driven M1 polarisation in macrophages. This attenuation of M1 polarisation correlates with reduced IL-6 secretion and the subsequent downregulation of the p -STAT3/HIF-1α/TFRC signalling axis, ultimately alleviating iron overload-associated oxidative stress.

    Article Snippet: For targeted osteoblast interventions, MC3T3-E1 cells were treated with the ferroptosis inhibitor Ferrostatin-1 (Fer-1; 10 μM, MedChemExpress, #HY-100579), an IL-6 neutralising antibody (1 μg/mL; Invitrogen, #16-7061-81), or the STAT3 specific inhibitor Stattic (5 μM; MedChemExpress, #HY-13818).

    Techniques:

    VPA-reprogrammed macrophage secretome rescues osteoblasts from ferroptosis via the IL-6/STAT3 axis. (A) CCK-8 assay assessing the viability of MC3T3-E1 cells treated with the indicated conditioned media or targeted inhibitors. (B) Viability of MC3T3-E1 cells treated with 100 ng/mL LPS for 24 h, to rule out direct endotoxin cytotoxicity. (C, D) Representative merged fluorescence images of JC-1 staining and corresponding quantitative analysis of the red/green fluorescence intensity ratio for evaluating mitochondrial membrane potential.(E) Representative merged fluorescence images of intracellular lipid peroxidation detected using the BODIPY 581/591 C11 probe.(F) Representative fluorescence images of the intracellular labile iron pool detected using the Phen Green SK probe.(G, H) Flow cytometry analysis of oxidised BODIPY 581/591 C11 (FITC channel), with representative stacked histograms and corresponding quantification of mean fluorescence intensity. (I) Intracellular GSH/GSSG ratio measured via biochemical assay. All quantitative data are presented as mean ± SD ( n = 3 independent biological replicates). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001 versus the LPS-CM group.

    Journal: Redox Report : Communications in Free Radical Research

    Article Title: Macrophage metabolic reprogramming via HIF-1α–glycolysis drives osteoblast ferroptosis and bone loss through an IL-6–STAT3–dependent redox axis

    doi: 10.1080/13510002.2026.2667673

    Figure Lengend Snippet: VPA-reprogrammed macrophage secretome rescues osteoblasts from ferroptosis via the IL-6/STAT3 axis. (A) CCK-8 assay assessing the viability of MC3T3-E1 cells treated with the indicated conditioned media or targeted inhibitors. (B) Viability of MC3T3-E1 cells treated with 100 ng/mL LPS for 24 h, to rule out direct endotoxin cytotoxicity. (C, D) Representative merged fluorescence images of JC-1 staining and corresponding quantitative analysis of the red/green fluorescence intensity ratio for evaluating mitochondrial membrane potential.(E) Representative merged fluorescence images of intracellular lipid peroxidation detected using the BODIPY 581/591 C11 probe.(F) Representative fluorescence images of the intracellular labile iron pool detected using the Phen Green SK probe.(G, H) Flow cytometry analysis of oxidised BODIPY 581/591 C11 (FITC channel), with representative stacked histograms and corresponding quantification of mean fluorescence intensity. (I) Intracellular GSH/GSSG ratio measured via biochemical assay. All quantitative data are presented as mean ± SD ( n = 3 independent biological replicates). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001 versus the LPS-CM group.

    Article Snippet: For targeted osteoblast interventions, MC3T3-E1 cells were treated with the ferroptosis inhibitor Ferrostatin-1 (Fer-1; 10 μM, MedChemExpress, #HY-100579), an IL-6 neutralising antibody (1 μg/mL; Invitrogen, #16-7061-81), or the STAT3 specific inhibitor Stattic (5 μM; MedChemExpress, #HY-13818).

    Techniques: CCK-8 Assay, Fluorescence, Staining, Membrane, Flow Cytometry

    Ultrastructural and mechanistic validation of the IL-6/STAT3-driven ferroptosis axis in osteoblasts. (A) Representative transmission electron microscopy (TEM) images of MC3T3-E1 osteoblasts exposed to the indicated treatments. Red arrows indicate typical ferroptotic mitochondria, characterised by reduced volume, increased membrane electron density, and disrupted cristae. (B, C) Representative Western blot images and corresponding quantitative densitometric analysis of p -STAT3 and total STAT3, demonstrating that IL-6 neutralising antibody (anti-IL-6) blocks upstream STAT3 activation. (D–H) Representative Western blot images and corresponding quantifications of ferroptosis-related proteins (TFRC, HIF-1α, GPX4, and ACSL4), revealing that the STAT3 inhibitor Stattic effectively reverses the molecular signature of ferroptosis. All quantitative data are presented as mean ± SD ( n = 3 independent biological replicates). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001 versus the LPS-CM group.

    Journal: Redox Report : Communications in Free Radical Research

    Article Title: Macrophage metabolic reprogramming via HIF-1α–glycolysis drives osteoblast ferroptosis and bone loss through an IL-6–STAT3–dependent redox axis

    doi: 10.1080/13510002.2026.2667673

    Figure Lengend Snippet: Ultrastructural and mechanistic validation of the IL-6/STAT3-driven ferroptosis axis in osteoblasts. (A) Representative transmission electron microscopy (TEM) images of MC3T3-E1 osteoblasts exposed to the indicated treatments. Red arrows indicate typical ferroptotic mitochondria, characterised by reduced volume, increased membrane electron density, and disrupted cristae. (B, C) Representative Western blot images and corresponding quantitative densitometric analysis of p -STAT3 and total STAT3, demonstrating that IL-6 neutralising antibody (anti-IL-6) blocks upstream STAT3 activation. (D–H) Representative Western blot images and corresponding quantifications of ferroptosis-related proteins (TFRC, HIF-1α, GPX4, and ACSL4), revealing that the STAT3 inhibitor Stattic effectively reverses the molecular signature of ferroptosis. All quantitative data are presented as mean ± SD ( n = 3 independent biological replicates). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001 versus the LPS-CM group.

    Article Snippet: For targeted osteoblast interventions, MC3T3-E1 cells were treated with the ferroptosis inhibitor Ferrostatin-1 (Fer-1; 10 μM, MedChemExpress, #HY-100579), an IL-6 neutralising antibody (1 μg/mL; Invitrogen, #16-7061-81), or the STAT3 specific inhibitor Stattic (5 μM; MedChemExpress, #HY-13818).

    Techniques: Biomarker Discovery, Transmission Assay, Electron Microscopy, Membrane, Western Blot, Activation Assay

    CKAP2L promotes proliferation and migration of colorectal cancer cells through the STAT3/AREG/EGFR axis. (A) Expression levels of STAT3 and p-STAT3 proteins measured by western blotting. (B) Calculation of IC 50 in HCT116 cells treated with Stattic for 24 h. (C) Levels of AREG were measured by reverse transcription-quantitative PCR and enzyme-linked immunosorbent assay. (D) Migration of cells was detected by Transwell assay (×100 magnification). (E) Proliferation of cells was measured by Cell Counting Kit 8. (F) Expression levels of proteins measured by western blotting. (G) Binding peak of STAT3 on the promoter region of AREG was detected by Cistrome Data Browser, the binding motif was predicted using the JASPAR database, and the binding of STAT3 to the AREG promoter was evaluated by chromatin immunoprecipitation assay. Data were analyzed using (A and G) Unpaired Student's t-test, and (C-F) two-way ANOVA followed by Tukey test. * P<0.05, ** P<0.01, *** P<0.001 and **** P<0.0001. AREG, amphiregulin; CKAP2L, cytoskeleton-associated protein 2-like; EGFR, epidermal growth factor receptor; NC, negative control; p-, phosphorylated; sh, short hairpin; STAT3, signal transducer and activator of transcription 3; TSS, transcription start site.

    Journal: International Journal of Oncology

    Article Title: Smoking promotes colorectal cancer via the CKAP2L/AREG axis

    doi: 10.3892/ijo.2026.5872

    Figure Lengend Snippet: CKAP2L promotes proliferation and migration of colorectal cancer cells through the STAT3/AREG/EGFR axis. (A) Expression levels of STAT3 and p-STAT3 proteins measured by western blotting. (B) Calculation of IC 50 in HCT116 cells treated with Stattic for 24 h. (C) Levels of AREG were measured by reverse transcription-quantitative PCR and enzyme-linked immunosorbent assay. (D) Migration of cells was detected by Transwell assay (×100 magnification). (E) Proliferation of cells was measured by Cell Counting Kit 8. (F) Expression levels of proteins measured by western blotting. (G) Binding peak of STAT3 on the promoter region of AREG was detected by Cistrome Data Browser, the binding motif was predicted using the JASPAR database, and the binding of STAT3 to the AREG promoter was evaluated by chromatin immunoprecipitation assay. Data were analyzed using (A and G) Unpaired Student's t-test, and (C-F) two-way ANOVA followed by Tukey test. * P<0.05, ** P<0.01, *** P<0.001 and **** P<0.0001. AREG, amphiregulin; CKAP2L, cytoskeleton-associated protein 2-like; EGFR, epidermal growth factor receptor; NC, negative control; p-, phosphorylated; sh, short hairpin; STAT3, signal transducer and activator of transcription 3; TSS, transcription start site.

    Article Snippet: The signal transducer and activator of transcription 3 (STAT3) phosphorylation inhibitor Stattic (cat. no. HY-13818; MedChemExpress) was dissolved in DMSO for cell culture.

    Techniques: Migration, Expressing, Western Blot, Reverse Transcription, Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay, Transwell Assay, Cell Counting, Binding Assay, Chromatin Immunoprecipitation, Negative Control

    Smoking may promote colorectal cancer progression through the CKAP2L/STAT3/AREG/EGFR axis. This figure was drawn by Figdraw ( https://www.figdraw.com/ ). AREG, amphiregulin; CKAP2L, cytoskeleton-associated protein 2-like; EGFR, epidermal growth factor receptor; STAT3, signal transducer and activator of transcription 3.

    Journal: International Journal of Oncology

    Article Title: Smoking promotes colorectal cancer via the CKAP2L/AREG axis

    doi: 10.3892/ijo.2026.5872

    Figure Lengend Snippet: Smoking may promote colorectal cancer progression through the CKAP2L/STAT3/AREG/EGFR axis. This figure was drawn by Figdraw ( https://www.figdraw.com/ ). AREG, amphiregulin; CKAP2L, cytoskeleton-associated protein 2-like; EGFR, epidermal growth factor receptor; STAT3, signal transducer and activator of transcription 3.

    Article Snippet: The signal transducer and activator of transcription 3 (STAT3) phosphorylation inhibitor Stattic (cat. no. HY-13818; MedChemExpress) was dissolved in DMSO for cell culture.

    Techniques: