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lysis buffer 17  (R&D Systems)


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    R&D Systems lysis buffer 17
    Lysis Buffer 17, supplied by R&D Systems, used in various techniques. Bioz Stars score: 96/100, based on 358 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+phospho+rtk+array+kit/Proteome+Profiler+Human+Phospho-RTK+Array+Kit/pm37676252-306-34-37
    Average 96 stars, based on 358 article reviews
    lysis buffer 17 - by Bioz Stars, 2026-09
    96/100 stars

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    Expressing:

    Article Title: Inhibition of nuclear ROCK2 by a novel thiourea derivative induces potent antitumor effects through PTEN/FOXO1 pathway restoration in prostate cancer.
    Article Snippet: Signal detection was performed using the Azure C300 Chemiluminescent Western Blot Imaging System (Azure Biosystems), and spot intensities were quantified using ImageJ software with the Protein Array Analyzer plugin. .. To assess the expression of multiple phosphorylated receptor tyrosine kinases (p-RTKs) in PANC-1, PC-3 and LNCaP cells, a membranebased antibody array was performed using Proteome Profiler Human p-RTK Array Kit (ARY001B; R&D system, Minneapolis, MN, USA). ..

    Ab Array:

    Article Title: Inhibition of nuclear ROCK2 by a novel thiourea derivative induces potent antitumor effects through PTEN/FOXO1 pathway restoration in prostate cancer.
    Article Snippet: Signal detection was performed using the Azure C300 Chemiluminescent Western Blot Imaging System (Azure Biosystems), and spot intensities were quantified using ImageJ software with the Protein Array Analyzer plugin. .. To assess the expression of multiple phosphorylated receptor tyrosine kinases (p-RTKs) in PANC-1, PC-3 and LNCaP cells, a membranebased antibody array was performed using Proteome Profiler Human p-RTK Array Kit (ARY001B; R&D system, Minneapolis, MN, USA). ..

    Activity Assay:

    Article Title: Extract of
    Article Snippet: Mapping of these targets was obtained with the aid of two antibody array kits which use a cellulose membrane on which antibodies are printed to detect the presence of proteins of interest (Proteome profiler human array kit, R&D Systems). .. The list of pharmacological targets screened in these tests is as follows and is available online: 49 phospho-receptors with tyrosine kinase activity (https://www.rndsystems.com/products/proteome-profiler-human-phospho-rtk-array-kit_ary001b) 43 signalling phosphokinases (https://www.rndsystems.com/products/proteome-profiler-human phospho-kinase-array-kit_ary003b#product-datasheets). .. The chemoluminescent signals were then detected using a densitometer (ChemiDoc, Biorad) and quantified with Image J 1.52 software using a Microarray profile plugin.

    Phospho-proteomics:

    Article Title: Inhibition of PREX1 Reverses Enzalutamide Resistance in Castration-Resistant Prostate Cancer.
    Article Snippet: The relative phosphorylation levels of selected signaling molecules were analyzed using two commercially available phosphoprotein arrays (R&D Systems). .. The Proteome Profiler Human Phospho-RTK Array Kit (cat. # ARY001B; R&D Systems) was designed for the parallel detection of the activities of 49 RTKs, and the Proteome Profiler Human Phospho-Kinase Array Kit (cat. # ARY003C; R&D Systems) was designed for the parallel detection of phosphorylation at 37 kinase phosphorylation sites and two related total proteins, all without performing immunoprecipitation or western blotting. .. Cell lysates were collected using Lysis Buffers 17 and 6 (both R&D Systems) for the Phospho-RTK and Phospho-Kinase Array Kits, respectively.

    Immunoprecipitation:

    Article Title: Inhibition of PREX1 Reverses Enzalutamide Resistance in Castration-Resistant Prostate Cancer.
    Article Snippet: The relative phosphorylation levels of selected signaling molecules were analyzed using two commercially available phosphoprotein arrays (R&D Systems). .. The Proteome Profiler Human Phospho-RTK Array Kit (cat. # ARY001B; R&D Systems) was designed for the parallel detection of the activities of 49 RTKs, and the Proteome Profiler Human Phospho-Kinase Array Kit (cat. # ARY003C; R&D Systems) was designed for the parallel detection of phosphorylation at 37 kinase phosphorylation sites and two related total proteins, all without performing immunoprecipitation or western blotting. .. Cell lysates were collected using Lysis Buffers 17 and 6 (both R&D Systems) for the Phospho-RTK and Phospho-Kinase Array Kits, respectively.

    Western Blot:

    Article Title: Inhibition of PREX1 Reverses Enzalutamide Resistance in Castration-Resistant Prostate Cancer.
    Article Snippet: The relative phosphorylation levels of selected signaling molecules were analyzed using two commercially available phosphoprotein arrays (R&D Systems). .. The Proteome Profiler Human Phospho-RTK Array Kit (cat. # ARY001B; R&D Systems) was designed for the parallel detection of the activities of 49 RTKs, and the Proteome Profiler Human Phospho-Kinase Array Kit (cat. # ARY003C; R&D Systems) was designed for the parallel detection of phosphorylation at 37 kinase phosphorylation sites and two related total proteins, all without performing immunoprecipitation or western blotting. .. Cell lysates were collected using Lysis Buffers 17 and 6 (both R&D Systems) for the Phospho-RTK and Phospho-Kinase Array Kits, respectively.

    Activation Assay:

    Article Title: Mutation-Resolved Drug Sensitivity Atlas Reveals Broad RAS(ON) Inhibitor Vulnerabilities and a STAT3 Co-Dependency in NRAS-Mutant Melanoma
    Article Snippet: .. RTK activation was evaluated using the Proteome ProfilerTM Human Phospho-RTK Array Kit (R&D Systems, Cat. No. ARY001B). ..

    Lysis:

    Article Title: An intestinal matrix-based human lung cancer model reflects clinical data from gefitinib on dosage-dependent efficacy.
    Article Snippet: Lung cancer is the leading cause for cancer related death worldwide.. One treatment option for patients with pulmonary adenocarcinoma is the targeted therapy gefitinib (Iressa®, ZD1839).. As with other promising targeted therapies, desired in vivo effects of gefitinib came short to in vitro expectations, as preclinical testing is hampered by an inaccuracy of existing models and resistances develop frequently.



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    STAT3 is required for survival of melanoma cells treated with active RAS(ON) inhibitors. (A) Signaling responses to RAS(ON) inhibition in isogenic MeWo cells expressing WT, Q61R, Q61K, or Q61L NRAS. Bubble plot summarizing Western blot–derived signaling changes after 8-hour treatment with the indicated inhibitors. Band intensities were quantified by densitometry, normalized to vehicle controls (set to 100%), and represented as bubble size. Cells were treated with dose ranges appropriate for each inhibitor class: sotorasib and adagrasib (0.1, 1, 10 μM); ADT-007, BI-2865, RMC-6236, and RMC-7977 (0.01, 0.1, 1, 10 μM). (B) Western blot analysis of phospho-STAT3 (Tyr705) in MeWo isogenic cells treated with 1 μM RMC-6236 or RMC-7977 for 0, 12, or 24 hours. (C) Apoptosis followed by STAT3 knockdown combined with RAS(ON) inhibition. (i) Representative Annexin V–FITC/PI density plot of MeWo NRAS WT , NRAS Q61R , NRAS Q61K , and NRAS Q61L cells treated for 48 hours with 1 μM RMC-6236, 1 μM RMC-7977, or DMSO. Red gate denotes apoptotic cells (Annexin VL). (ii) Quantification of total apoptotic cells. Data are presented as mean ± SD (n = 3). Statistical significance was assessed using Two-way ANOVA with Sidak’s multiple-comparisons test (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001). (D) Western blot of MYC, p-STAT3, and cleaved PARP following siSTAT3 combined with 24-hour treatment with 1 μM RMC-6236 or RMC-7977. From (A) to (D), data were confirmed with independent experiments. (E) Receptor Tyrosine Kinase activation following RAS(ON) inhibitor treatment. (i) <t>Representative</t> <t>phospho-RTK</t> array from NRAS Q61R MeWo cells treated with 1 μM RMC-6236 or vehicle for 18 hours. (ii) Quantification of significantly upregulated RTKs. Data are mean ± SD. Statistical significance was determined by Two-way ANOVA with Sidak’s multiple-comparisons test (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001).
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    STAT3 is required for survival of melanoma cells treated with active RAS(ON) inhibitors. (A) Signaling responses to RAS(ON) inhibition in isogenic MeWo cells expressing WT, Q61R, Q61K, or Q61L NRAS. Bubble plot summarizing Western blot–derived signaling changes after 8-hour treatment with the indicated inhibitors. Band intensities were quantified by densitometry, normalized to vehicle controls (set to 100%), and represented as bubble size. Cells were treated with dose ranges appropriate for each inhibitor class: sotorasib and adagrasib (0.1, 1, 10 μM); ADT-007, BI-2865, RMC-6236, and RMC-7977 (0.01, 0.1, 1, 10 μM). (B) Western blot analysis of phospho-STAT3 (Tyr705) in MeWo isogenic cells treated with 1 μM RMC-6236 or RMC-7977 for 0, 12, or 24 hours. (C) Apoptosis followed by STAT3 knockdown combined with RAS(ON) inhibition. (i) Representative Annexin V–FITC/PI density plot of MeWo NRAS WT , NRAS Q61R , NRAS Q61K , and NRAS Q61L cells treated for 48 hours with 1 μM RMC-6236, 1 μM RMC-7977, or DMSO. Red gate denotes apoptotic cells (Annexin VL). (ii) Quantification of total apoptotic cells. Data are presented as mean ± SD (n = 3). Statistical significance was assessed using Two-way ANOVA with Sidak’s multiple-comparisons test (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001). (D) Western blot of MYC, p-STAT3, and cleaved PARP following siSTAT3 combined with 24-hour treatment with 1 μM RMC-6236 or RMC-7977. From (A) to (D), data were confirmed with independent experiments. (E) Receptor Tyrosine Kinase activation following RAS(ON) inhibitor treatment. (i) <t>Representative</t> <t>phospho-RTK</t> array from NRAS Q61R MeWo cells treated with 1 μM RMC-6236 or vehicle for 18 hours. (ii) Quantification of significantly upregulated RTKs. Data are mean ± SD. Statistical significance was determined by Two-way ANOVA with Sidak’s multiple-comparisons test (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001).
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    STAT3 is required for survival of melanoma cells treated with active RAS(ON) inhibitors. (A) Signaling responses to RAS(ON) inhibition in isogenic MeWo cells expressing WT, Q61R, Q61K, or Q61L NRAS. Bubble plot summarizing Western blot–derived signaling changes after 8-hour treatment with the indicated inhibitors. Band intensities were quantified by densitometry, normalized to vehicle controls (set to 100%), and represented as bubble size. Cells were treated with dose ranges appropriate for each inhibitor class: sotorasib and adagrasib (0.1, 1, 10 μM); ADT-007, BI-2865, RMC-6236, and RMC-7977 (0.01, 0.1, 1, 10 μM). (B) Western blot analysis of phospho-STAT3 (Tyr705) in MeWo isogenic cells treated with 1 μM RMC-6236 or RMC-7977 for 0, 12, or 24 hours. (C) Apoptosis followed by STAT3 knockdown combined with RAS(ON) inhibition. (i) Representative Annexin V–FITC/PI density plot of MeWo NRAS WT , NRAS Q61R , NRAS Q61K , and NRAS Q61L cells treated for 48 hours with 1 μM RMC-6236, 1 μM RMC-7977, or DMSO. Red gate denotes apoptotic cells (Annexin VL). (ii) Quantification of total apoptotic cells. Data are presented as mean ± SD (n = 3). Statistical significance was assessed using Two-way ANOVA with Sidak’s multiple-comparisons test (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001). (D) Western blot of MYC, p-STAT3, and cleaved PARP following siSTAT3 combined with 24-hour treatment with 1 μM RMC-6236 or RMC-7977. From (A) to (D), data were confirmed with independent experiments. (E) Receptor Tyrosine Kinase activation following RAS(ON) inhibitor treatment. (i) <t>Representative</t> <t>phospho-RTK</t> array from NRAS Q61R MeWo cells treated with 1 μM RMC-6236 or vehicle for 18 hours. (ii) Quantification of significantly upregulated RTKs. Data are mean ± SD. Statistical significance was determined by Two-way ANOVA with Sidak’s multiple-comparisons test (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001).
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    Image Search Results


    STAT3 is required for survival of melanoma cells treated with active RAS(ON) inhibitors. (A) Signaling responses to RAS(ON) inhibition in isogenic MeWo cells expressing WT, Q61R, Q61K, or Q61L NRAS. Bubble plot summarizing Western blot–derived signaling changes after 8-hour treatment with the indicated inhibitors. Band intensities were quantified by densitometry, normalized to vehicle controls (set to 100%), and represented as bubble size. Cells were treated with dose ranges appropriate for each inhibitor class: sotorasib and adagrasib (0.1, 1, 10 μM); ADT-007, BI-2865, RMC-6236, and RMC-7977 (0.01, 0.1, 1, 10 μM). (B) Western blot analysis of phospho-STAT3 (Tyr705) in MeWo isogenic cells treated with 1 μM RMC-6236 or RMC-7977 for 0, 12, or 24 hours. (C) Apoptosis followed by STAT3 knockdown combined with RAS(ON) inhibition. (i) Representative Annexin V–FITC/PI density plot of MeWo NRAS WT , NRAS Q61R , NRAS Q61K , and NRAS Q61L cells treated for 48 hours with 1 μM RMC-6236, 1 μM RMC-7977, or DMSO. Red gate denotes apoptotic cells (Annexin VL). (ii) Quantification of total apoptotic cells. Data are presented as mean ± SD (n = 3). Statistical significance was assessed using Two-way ANOVA with Sidak’s multiple-comparisons test (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001). (D) Western blot of MYC, p-STAT3, and cleaved PARP following siSTAT3 combined with 24-hour treatment with 1 μM RMC-6236 or RMC-7977. From (A) to (D), data were confirmed with independent experiments. (E) Receptor Tyrosine Kinase activation following RAS(ON) inhibitor treatment. (i) Representative phospho-RTK array from NRAS Q61R MeWo cells treated with 1 μM RMC-6236 or vehicle for 18 hours. (ii) Quantification of significantly upregulated RTKs. Data are mean ± SD. Statistical significance was determined by Two-way ANOVA with Sidak’s multiple-comparisons test (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001).

    Journal: bioRxiv

    Article Title: Mutation-Resolved Drug Sensitivity Atlas Reveals Broad RAS(ON) Inhibitor Vulnerabilities and a STAT3 Co-Dependency in NRAS-Mutant Melanoma

    doi: 10.64898/2026.02.18.706707

    Figure Lengend Snippet: STAT3 is required for survival of melanoma cells treated with active RAS(ON) inhibitors. (A) Signaling responses to RAS(ON) inhibition in isogenic MeWo cells expressing WT, Q61R, Q61K, or Q61L NRAS. Bubble plot summarizing Western blot–derived signaling changes after 8-hour treatment with the indicated inhibitors. Band intensities were quantified by densitometry, normalized to vehicle controls (set to 100%), and represented as bubble size. Cells were treated with dose ranges appropriate for each inhibitor class: sotorasib and adagrasib (0.1, 1, 10 μM); ADT-007, BI-2865, RMC-6236, and RMC-7977 (0.01, 0.1, 1, 10 μM). (B) Western blot analysis of phospho-STAT3 (Tyr705) in MeWo isogenic cells treated with 1 μM RMC-6236 or RMC-7977 for 0, 12, or 24 hours. (C) Apoptosis followed by STAT3 knockdown combined with RAS(ON) inhibition. (i) Representative Annexin V–FITC/PI density plot of MeWo NRAS WT , NRAS Q61R , NRAS Q61K , and NRAS Q61L cells treated for 48 hours with 1 μM RMC-6236, 1 μM RMC-7977, or DMSO. Red gate denotes apoptotic cells (Annexin VL). (ii) Quantification of total apoptotic cells. Data are presented as mean ± SD (n = 3). Statistical significance was assessed using Two-way ANOVA with Sidak’s multiple-comparisons test (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001). (D) Western blot of MYC, p-STAT3, and cleaved PARP following siSTAT3 combined with 24-hour treatment with 1 μM RMC-6236 or RMC-7977. From (A) to (D), data were confirmed with independent experiments. (E) Receptor Tyrosine Kinase activation following RAS(ON) inhibitor treatment. (i) Representative phospho-RTK array from NRAS Q61R MeWo cells treated with 1 μM RMC-6236 or vehicle for 18 hours. (ii) Quantification of significantly upregulated RTKs. Data are mean ± SD. Statistical significance was determined by Two-way ANOVA with Sidak’s multiple-comparisons test (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001).

    Article Snippet: RTK activation was evaluated using the Proteome ProfilerTM Human Phospho-RTK Array Kit (R&D Systems, Cat. No. ARY001B).

    Techniques: Inhibition, Expressing, Western Blot, Derivative Assay, Knockdown, Activation Assay