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iressa  (Bio-Techne corporation)


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    Structured Review

    Bio-Techne corporation iressa
    Iressa, supplied by Bio-Techne corporation, used in various techniques. Bioz Stars score: 93/100, based on 363 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/iressa/Iressa/custom%403000%4042456009
    Average 93 stars, based on 363 article reviews
    iressa - by Bioz Stars, 2026-09
    93/100 stars

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    Related Articles

    Incubation:

    Article Title: An integrin beta-1-anchored bicaudal C1-polycystin-1 module essential for tubular morphogenesis in polycystic kidney disease
    Article Snippet: nson, UK), plated into 96 well plates in triplicate and incubated for 30 min at 37°C to facilitate gel formation. Cells were then cultured for 12days in the presence of vehicle (DMSO) or 50 μM CK-666 (Tocris, UK). Media was replaced every 2 days. The percentage of tubular structures was calculated from 3 independent wells per treatment. Cells were transfected using Lipofectamine 3000 (Life Technolo

    Transfection:

    Article Title: An integrin beta-1-anchored bicaudal C1-polycystin-1 module essential for tubular morphogenesis in polycystic kidney disease
    Article Snippet: nson, UK), plated into 96 well plates in triplicate and incubated for 30 min at 37°C to facilitate gel formation. Cells were then cultured for 12days in the presence of vehicle (DMSO) or 50 μM CK-666 (Tocris, UK). Media was replaced every 2 days. The percentage of tubular structures was calculated from 3 independent wells per treatment. Cells were transfected using Lipofectamine 3000 (Life Technolo

    Cell Culture:

    Article Title: An integrin beta-1-anchored bicaudal C1-polycystin-1 module essential for tubular morphogenesis in polycystic kidney disease
    Article Snippet: nson, UK), plated into 96 well plates in triplicate and incubated for 30 min at 37°C to facilitate gel formation. Cells were then cultured for 12days in the presence of vehicle (DMSO) or 50 μM CK-666 (Tocris, UK). Media was replaced every 2 days. The percentage of tubular structures was calculated from 3 independent wells per treatment. Cells were transfected using Lipofectamine 3000 (Life Technolo

    Electroporation:

    Article Title: An integrin beta-1-anchored bicaudal C1-polycystin-1 module essential for tubular morphogenesis in polycystic kidney disease
    Article Snippet: nson, UK), plated into 96 well plates in triplicate and incubated for 30 min at 37°C to facilitate gel formation. Cells were then cultured for 12days in the presence of vehicle (DMSO) or 50 μM CK-666 (Tocris, UK). Media was replaced every 2 days. The percentage of tubular structures was calculated from 3 independent wells per treatment. Cells were transfected using Lipofectamine 3000 (Life Technolo

    Staining:

    Article Title: An integrin beta-1-anchored bicaudal C1-polycystin-1 module essential for tubular morphogenesis in polycystic kidney disease
    Article Snippet: nson, UK), plated into 96 well plates in triplicate and incubated for 30 min at 37°C to facilitate gel formation. Cells were then cultured for 12days in the presence of vehicle (DMSO) or 50 μM CK-666 (Tocris, UK). Media was replaced every 2 days. The percentage of tubular structures was calculated from 3 independent wells per treatment. Cells were transfected using Lipofectamine 3000 (Life Technolo

    Positive Control:

    Article Title: An integrin beta-1-anchored bicaudal C1-polycystin-1 module essential for tubular morphogenesis in polycystic kidney disease
    Article Snippet: nson, UK), plated into 96 well plates in triplicate and incubated for 30 min at 37°C to facilitate gel formation. Cells were then cultured for 12days in the presence of vehicle (DMSO) or 50 μM CK-666 (Tocris, UK). Media was replaced every 2 days. The percentage of tubular structures was calculated from 3 independent wells per treatment. Cells were transfected using Lipofectamine 3000 (Life Technolo

    Immunostaining:

    Article Title: An integrin beta-1-anchored bicaudal C1-polycystin-1 module essential for tubular morphogenesis in polycystic kidney disease
    Article Snippet: nson, UK), plated into 96 well plates in triplicate and incubated for 30 min at 37°C to facilitate gel formation. Cells were then cultured for 12days in the presence of vehicle (DMSO) or 50 μM CK-666 (Tocris, UK). Media was replaced every 2 days. The percentage of tubular structures was calculated from 3 independent wells per treatment. Cells were transfected using Lipofectamine 3000 (Life Technolo

    Control:

    Article Title: An integrin beta-1-anchored bicaudal C1-polycystin-1 module essential for tubular morphogenesis in polycystic kidney disease
    Article Snippet: nson, UK), plated into 96 well plates in triplicate and incubated for 30 min at 37°C to facilitate gel formation. Cells were then cultured for 12days in the presence of vehicle (DMSO) or 50 μM CK-666 (Tocris, UK). Media was replaced every 2 days. The percentage of tubular structures was calculated from 3 independent wells per treatment. Cells were transfected using Lipofectamine 3000 (Life Technolo

    Inhibition:

    Article Title: An integrin beta-1-anchored bicaudal C1-polycystin-1 module essential for tubular morphogenesis in polycystic kidney disease
    Article Snippet: nson, UK), plated into 96 well plates in triplicate and incubated for 30 min at 37°C to facilitate gel formation. Cells were then cultured for 12days in the presence of vehicle (DMSO) or 50 μM CK-666 (Tocris, UK). Media was replaced every 2 days. The percentage of tubular structures was calculated from 3 independent wells per treatment. Cells were transfected using Lipofectamine 3000 (Life Technolo

    Plasmid Preparation:

    Article Title: An integrin beta-1-anchored bicaudal C1-polycystin-1 module essential for tubular morphogenesis in polycystic kidney disease
    Article Snippet: nson, UK), plated into 96 well plates in triplicate and incubated for 30 min at 37°C to facilitate gel formation. Cells were then cultured for 12days in the presence of vehicle (DMSO) or 50 μM CK-666 (Tocris, UK). Media was replaced every 2 days. The percentage of tubular structures was calculated from 3 independent wells per treatment. Cells were transfected using Lipofectamine 3000 (Life Technolo

    Imaging:

    Article Title: An integrin beta-1-anchored bicaudal C1-polycystin-1 module essential for tubular morphogenesis in polycystic kidney disease
    Article Snippet: nson, UK), plated into 96 well plates in triplicate and incubated for 30 min at 37°C to facilitate gel formation. Cells were then cultured for 12days in the presence of vehicle (DMSO) or 50 μM CK-666 (Tocris, UK). Media was replaced every 2 days. The percentage of tubular structures was calculated from 3 independent wells per treatment. Cells were transfected using Lipofectamine 3000 (Life Technolo



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    Image Search Results


    PDK1 inhibitor JX06 and gefitinib synergistically induced cell apoptosis in gefitinib-resistant lung cancer cells. (A) The protein expression levels of PDK were reduced upon the treatment of PDK1 inhibitor JX06 in PC-9 and PC-9/G cells. (B) B2B and PC-9/G cells were treated with different concentrations of JX06 for 48 h. The cell viabilities were determined by CCK-8. (C – E) The synergy effect between JX06 and gefitinib was determined and analyzed with CompuSyn software. (F) The apoptosis rates were analyzed with flow cytometry after the combined treatment of gefitinib and JX06. (G) The TUNEL assay was performed with the indicated treatment in PC-9/G cells. (H) The cells treated as described were stained with the JC-1 probe and detected using a fluorescence microscope. Red fluorescence indicates the aggregation form of JC-1, showing increased mitochondrial membrane potential (ΔΨm). Green fluorescence indicates the monomeric form of JC-1, which indicates reduced mitochondrial membrane potential (ΔΨm). Data were statistically analyzed with Student’s t -test, and values were shown as mean ± standard deviation. ∗ P < 0.05 and ∗∗ P < 0.01.

    Journal: Genes & Diseases

    Article Title: PDK1 elevation was induced by epigenetic modifications of KDM3A and METTL16 to mediate TKI resistance and cancer development

    doi: 10.1016/j.gendis.2025.101947

    Figure Lengend Snippet: PDK1 inhibitor JX06 and gefitinib synergistically induced cell apoptosis in gefitinib-resistant lung cancer cells. (A) The protein expression levels of PDK were reduced upon the treatment of PDK1 inhibitor JX06 in PC-9 and PC-9/G cells. (B) B2B and PC-9/G cells were treated with different concentrations of JX06 for 48 h. The cell viabilities were determined by CCK-8. (C – E) The synergy effect between JX06 and gefitinib was determined and analyzed with CompuSyn software. (F) The apoptosis rates were analyzed with flow cytometry after the combined treatment of gefitinib and JX06. (G) The TUNEL assay was performed with the indicated treatment in PC-9/G cells. (H) The cells treated as described were stained with the JC-1 probe and detected using a fluorescence microscope. Red fluorescence indicates the aggregation form of JC-1, showing increased mitochondrial membrane potential (ΔΨm). Green fluorescence indicates the monomeric form of JC-1, which indicates reduced mitochondrial membrane potential (ΔΨm). Data were statistically analyzed with Student’s t -test, and values were shown as mean ± standard deviation. ∗ P < 0.05 and ∗∗ P < 0.01.

    Article Snippet: Gefitinib and JX06 were purchased from MedChemExpress (Shanghai, China).

    Techniques: Expressing, CCK-8 Assay, Software, Flow Cytometry, TUNEL Assay, Staining, Fluorescence, Microscopy, Membrane, Standard Deviation

    Dual-treatment of JX06 and gefitinib significantly inhibited tumor growth in vivo . The PC-9/G cells (5 × 10 6 cells) were inoculated subcutaneously on the back of nude mice. When the tumor reached approximately 5 × 5 mm 2 , the nude mice were randomly divided into four groups ( n = 5 per group) and treated with saline, gefitinib (25 mg/kg), JX06 (30 mg/kg), or gefitinib (25 mg/kg) plus JX06 (30 mg/kg). (A – C) Tumor volumes and weights were analyzed, and dual-treatment of JX06 and gefitinib significantly inhibited tumor volumes and tumor weights. (D) Animal weights between the four groups did not show any significant difference. (E) Representative images of immunohistochemical staining of Ki67 and CD31 in paraffin-embedded xenograft tumor tissues, and the expression levels of Ki67 and CD31 were quantified for six microscopic fields of the tumor samples. Data were statistically analyzed with Student’s t -test, and values were shown as mean ± standard deviation. ∗ P < 0.05 and ∗∗ P < 0.01.

    Journal: Genes & Diseases

    Article Title: PDK1 elevation was induced by epigenetic modifications of KDM3A and METTL16 to mediate TKI resistance and cancer development

    doi: 10.1016/j.gendis.2025.101947

    Figure Lengend Snippet: Dual-treatment of JX06 and gefitinib significantly inhibited tumor growth in vivo . The PC-9/G cells (5 × 10 6 cells) were inoculated subcutaneously on the back of nude mice. When the tumor reached approximately 5 × 5 mm 2 , the nude mice were randomly divided into four groups ( n = 5 per group) and treated with saline, gefitinib (25 mg/kg), JX06 (30 mg/kg), or gefitinib (25 mg/kg) plus JX06 (30 mg/kg). (A – C) Tumor volumes and weights were analyzed, and dual-treatment of JX06 and gefitinib significantly inhibited tumor volumes and tumor weights. (D) Animal weights between the four groups did not show any significant difference. (E) Representative images of immunohistochemical staining of Ki67 and CD31 in paraffin-embedded xenograft tumor tissues, and the expression levels of Ki67 and CD31 were quantified for six microscopic fields of the tumor samples. Data were statistically analyzed with Student’s t -test, and values were shown as mean ± standard deviation. ∗ P < 0.05 and ∗∗ P < 0.01.

    Article Snippet: Gefitinib and JX06 were purchased from MedChemExpress (Shanghai, China).

    Techniques: In Vivo, Saline, Immunohistochemical staining, Staining, Expressing, Standard Deviation