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epidermal growth factor receptor egfr kinase inhibitor ag1478  (MedChemExpress)


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    MedChemExpress epidermal growth factor receptor egfr kinase inhibitor ag1478
    Epidermal Growth Factor Receptor Egfr Kinase Inhibitor Ag1478, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 76 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ag+1478/AG-1478/pm42858920-61-0-10
    Average 95 stars, based on 76 article reviews
    epidermal growth factor receptor egfr kinase inhibitor ag1478 - by Bioz Stars, 2026-11
    95/100 stars

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    Blocking Assay:

    Article Title: Recombinant tissue plasminogen activator protects neurons after intracerebral hemorrhage through activating the PI3K/AKT/mTOR pathway
    Article Snippet: .. Different inhibitors dissolved in culture medium were applied to block specific domains: 300 nM GGACK (34618, Cayman Chemical Company, MI, USA) to block the protease domain, 500 nM receptor-associated protein (RAP; an inhibitor of LRP; 50281- M08H, Sino Biological, Beijing, China) to block the effect of the finger domain, 5 μM AG-1478 (an inhibitor of the EGF receptor; HY13524-10, MCE, Shanghai, China) to block the function of EGF domain, and 300 nM tranexamic acid (TXA; HY-B0149-5, MCE) to block a target on the Kringle domain (n = 3/group). .. Specific pathogen-free C57BL/6J mice were provided by the Experimental Animal Center of Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology (Wuhan, China; Animal License No. SCXK (E) 2021-0009).

    Article Title: Recombinant tissue plasminogen activator protects neurons after intracerebral hemorrhage through activating the PI3K/AKT/mTOR pathway
    Article Snippet: .. Different inhibitors dissolved in culture medium were applied to block specific domains: 300 nM GGACK (34618, Cayman Chemical Company, MI, USA) to block the protease domain, 500 nM receptor-associated protein (RAP; an inhibitor of LRP; 50281-M08H, Sino Biological, Beijing, China) to block the effect of the finger domain, 5 μM AG-1478 (an inhibitor of the EGF receptor; HY13524-10, MCE, Shanghai, China) to block the function of EGF domain, and 300 nM tranexamic acid (TXA; HY-B0149-5, MCE) to block a target on the Kringle domain ( n = 3/group). .. Specific pathogen-free C57BL/6J mice were provided by the Experimental Animal Center of Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology (Wuhan, China; Animal License No. SCXK (E) 2021-0009).

    Indirect Immunoperoxidase Assay:

    Article Title: RABV induces biphasic actin cytoskeletal rearrangement through Rac1 activity modulation
    Article Snippet: Pharmacological inhibitors were dissolved in dimethyl sulfoxide (DMSO; V900090, Sigma) or DMEM medium following the manufacturer’s recommendation and used at indicated concentration. .. Latrunculin A (Lat A; ab144290, Abcam), Jasplakinolide (Jasp; 141409, Abcam), CCG-1423(S7719, Selleck), ML141(HY-12755, MCE), AG-1478 (HY-13524, MCE), Wortmannin (HY-10197, MCE), AKT VIII (HY-10355, MCE), NSC23766 (S8031, Selleck), and IPA-3 (HY-15663, MCE) were employed. .. Antibodies used are as follows: Fluorescein isothiocyanate anti-Rabies Monoclonal globulin antibody (800–092, FUJIREBIO), anti-Flag (8146S, Cell Signaling Technology), anti-Rabies Virus (5B12; NB110–7542, Novus), anti-RhoA (2117S, Cell Signaling Technology), anti-Cdc42 (2462S, Cell Signaling Technology), anti-Rac1 (ab282581, Abcam), anti-GFP(66002–1-lg, Proteintech), anti-EGFR (4267S, Cell Signaling Technology), anti-p-EGFR (3777S, Cell Signaling Technology), anti-PI3K (66225–1-lg, Proteintech), anti-p-PI3K (17366S, Cell Signaling Technology), anti-Akt (10176–2-AP, Proteintech), anti-p-Akt (66444–1-lg, Proteintech), anti-Pak1 (2601S, Cell Signaling Technology), anti-p-Pak1 (D155068, BBI LIFE SCIENCES), anti-Limk1 (3842S, Cell Signaling Technology), anti-p-Limk1 (YP0591, IMMUNOWAY), anti-Cofilin1 (ab428424, Abcam), anti-p-Cofilin1 (3313S, Cell Signaling Technology), anti-GAPDH (1A6; MB001, Bioworld), horseradish peroxidase (HRP)-labeled goat anti-mouse antibody (AP308P, Sigma), and HRP-conjugated goat anti-Rabbit IgG (SA00001-2, Proteintech).



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    IL-37/IL-1R8 protects HaCaT cells from keratinocyte dissociation and apoptosis through the ADAM17/EGFR pathway. (A) Protein expression levels of ADAM17, p-EGFR, total EGFR as well as EGFR downstream protein p-AKT, p-ERK1/2 and p-STAT3 levels were determined by western blotting. HaCaT cells were treated with EGFR activator NSC228155. (B) Cell dissociation was analyzed by cell dissociation assay. (C) Cell apoptosis was analyzed by flow cytometry. (D) Protein expression levels of Bcl-2 and Bax were analyzed by western blotting. (E) HaCaT was transfected with ADAM17 siRNA and the transfection efficiency was detected by western blotting. HaCaT cells were transfected with ADAM17 siRNA or treated with 1 μ M of EGFR inhibitor <t>AG1478</t> for 30 min followed by treated with AK23. (F) Cell dissociation was analyzed by cell dissociation assay. (G) Cell apoptosis was analyzed by flow cytometry. # P<0.05 vs. Control group; & P<0.05 vs. anti-Dsg3 group; @ P<0.05 vs. anti- Dsg3 + IL-37 + si-NC group; * P<0.05; Data are presented as mean ± SD, n=3 biological indepen- dent replicates. One-way ANOVA with Bonferroni's post-hoc test was used for multiple group comparisons. IL, interleukin; ADAM17, TNF-alpha-converting enzyme; EGFR, epidermal growth factor receptor; p- phosphorylated; STAT, signal transducer and activator of transcription; si, short interfering.
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    IL-37/IL-1R8 protects HaCaT cells from keratinocyte dissociation and apoptosis through the ADAM17/EGFR pathway. (A) Protein expression levels of ADAM17, p-EGFR, total EGFR as well as EGFR downstream protein p-AKT, p-ERK1/2 and p-STAT3 levels were determined by western blotting. HaCaT cells were treated with EGFR activator NSC228155. (B) Cell dissociation was analyzed by cell dissociation assay. (C) Cell apoptosis was analyzed by flow cytometry. (D) Protein expression levels of Bcl-2 and Bax were analyzed by western blotting. (E) HaCaT was transfected with ADAM17 siRNA and the transfection efficiency was detected by western blotting. HaCaT cells were transfected with ADAM17 siRNA or treated with 1 μ M of EGFR inhibitor <t>AG1478</t> for 30 min followed by treated with AK23. (F) Cell dissociation was analyzed by cell dissociation assay. (G) Cell apoptosis was analyzed by flow cytometry. # P<0.05 vs. Control group; & P<0.05 vs. anti-Dsg3 group; @ P<0.05 vs. anti- Dsg3 + IL-37 + si-NC group; * P<0.05; Data are presented as mean ± SD, n=3 biological indepen- dent replicates. One-way ANOVA with Bonferroni's post-hoc test was used for multiple group comparisons. IL, interleukin; ADAM17, TNF-alpha-converting enzyme; EGFR, epidermal growth factor receptor; p- phosphorylated; STAT, signal transducer and activator of transcription; si, short interfering.
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    IL-37/IL-1R8 protects HaCaT cells from keratinocyte dissociation and apoptosis through the ADAM17/EGFR pathway. (A) Protein expression levels of ADAM17, p-EGFR, total EGFR as well as EGFR downstream protein p-AKT, p-ERK1/2 and p-STAT3 levels were determined by western blotting. HaCaT cells were treated with EGFR activator NSC228155. (B) Cell dissociation was analyzed by cell dissociation assay. (C) Cell apoptosis was analyzed by flow cytometry. (D) Protein expression levels of Bcl-2 and Bax were analyzed by western blotting. (E) HaCaT was transfected with ADAM17 siRNA and the transfection efficiency was detected by western blotting. HaCaT cells were transfected with ADAM17 siRNA or treated with 1 μ M of EGFR inhibitor <t>AG1478</t> for 30 min followed by treated with AK23. (F) Cell dissociation was analyzed by cell dissociation assay. (G) Cell apoptosis was analyzed by flow cytometry. # P<0.05 vs. Control group; & P<0.05 vs. anti-Dsg3 group; @ P<0.05 vs. anti- Dsg3 + IL-37 + si-NC group; * P<0.05; Data are presented as mean ± SD, n=3 biological indepen- dent replicates. One-way ANOVA with Bonferroni's post-hoc test was used for multiple group comparisons. IL, interleukin; ADAM17, TNF-alpha-converting enzyme; EGFR, epidermal growth factor receptor; p- phosphorylated; STAT, signal transducer and activator of transcription; si, short interfering.
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    Image Search Results


    IL-37/IL-1R8 protects HaCaT cells from keratinocyte dissociation and apoptosis through the ADAM17/EGFR pathway. (A) Protein expression levels of ADAM17, p-EGFR, total EGFR as well as EGFR downstream protein p-AKT, p-ERK1/2 and p-STAT3 levels were determined by western blotting. HaCaT cells were treated with EGFR activator NSC228155. (B) Cell dissociation was analyzed by cell dissociation assay. (C) Cell apoptosis was analyzed by flow cytometry. (D) Protein expression levels of Bcl-2 and Bax were analyzed by western blotting. (E) HaCaT was transfected with ADAM17 siRNA and the transfection efficiency was detected by western blotting. HaCaT cells were transfected with ADAM17 siRNA or treated with 1 μ M of EGFR inhibitor AG1478 for 30 min followed by treated with AK23. (F) Cell dissociation was analyzed by cell dissociation assay. (G) Cell apoptosis was analyzed by flow cytometry. # P<0.05 vs. Control group; & P<0.05 vs. anti-Dsg3 group; @ P<0.05 vs. anti- Dsg3 + IL-37 + si-NC group; * P<0.05; Data are presented as mean ± SD, n=3 biological indepen- dent replicates. One-way ANOVA with Bonferroni's post-hoc test was used for multiple group comparisons. IL, interleukin; ADAM17, TNF-alpha-converting enzyme; EGFR, epidermal growth factor receptor; p- phosphorylated; STAT, signal transducer and activator of transcription; si, short interfering.

    Journal: International Journal of Molecular Medicine

    Article Title: IL-37/IL-1R8 blocks keratinocyte acantholysis via suppressing ADAM17/EGFR

    doi: 10.3892/ijmm.2026.5793

    Figure Lengend Snippet: IL-37/IL-1R8 protects HaCaT cells from keratinocyte dissociation and apoptosis through the ADAM17/EGFR pathway. (A) Protein expression levels of ADAM17, p-EGFR, total EGFR as well as EGFR downstream protein p-AKT, p-ERK1/2 and p-STAT3 levels were determined by western blotting. HaCaT cells were treated with EGFR activator NSC228155. (B) Cell dissociation was analyzed by cell dissociation assay. (C) Cell apoptosis was analyzed by flow cytometry. (D) Protein expression levels of Bcl-2 and Bax were analyzed by western blotting. (E) HaCaT was transfected with ADAM17 siRNA and the transfection efficiency was detected by western blotting. HaCaT cells were transfected with ADAM17 siRNA or treated with 1 μ M of EGFR inhibitor AG1478 for 30 min followed by treated with AK23. (F) Cell dissociation was analyzed by cell dissociation assay. (G) Cell apoptosis was analyzed by flow cytometry. # P<0.05 vs. Control group; & P<0.05 vs. anti-Dsg3 group; @ P<0.05 vs. anti- Dsg3 + IL-37 + si-NC group; * P<0.05; Data are presented as mean ± SD, n=3 biological indepen- dent replicates. One-way ANOVA with Bonferroni's post-hoc test was used for multiple group comparisons. IL, interleukin; ADAM17, TNF-alpha-converting enzyme; EGFR, epidermal growth factor receptor; p- phosphorylated; STAT, signal transducer and activator of transcription; si, short interfering.

    Article Snippet: For EGFR inhibition assay, HaCaT cells were pre-treated with 1 μ M of EGFR inhibitor AG1478 (MedChemExpress) at 37°C for 30 min followed by treatment with AK23 for 24 h at 37°C.

    Techniques: Expressing, Western Blot, Flow Cytometry, Transfection, Control