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proteome profilertm human phospho rtk array kit  (R&D Systems)


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    R&D Systems proteome profilertm human phospho rtk array kit
    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).
    Proteome Profilertm Human Phospho Rtk Array Kit, 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/proteome+profilertm+human+phospho+rtk+array+kit/Proteome+Profiler+Human+Phospho-RTK+Array+Kit/bio_rxiv__64898__2026__02__18__706707-193-6-12
    Average 96 stars, based on 358 article reviews
    proteome profilertm human phospho rtk array kit - by Bioz Stars, 2026-09
    96/100 stars

    Images

    1) Product Images from "Mutation-Resolved Drug Sensitivity Atlas Reveals Broad RAS(ON) Inhibitor Vulnerabilities and a STAT3 Co-Dependency in NRAS-Mutant Melanoma"

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

    Journal: bioRxiv

    doi: 10.64898/2026.02.18.706707

    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).
    Figure Legend 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).

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

    Related Articles

    Phospho-proteomics:

    Article Title: Thiosemicarbazones and selected tyrosine kinase inhibitors synergize in pediatric solid tumors: NDRG1 upregulation and impaired prosurvival signaling in neuroblastoma cells
    Article Snippet: .. The relative levels of phosphorylation of 49 RTKs ( ) were assayed using a Proteome ProfilerTM human phospho-RTK array kit (cat. no. ARY001B) purchased from R&D Systems (Minneapolis, MN, United States). ..

    Article Title: Stellettin B Induces Cell Death in Bladder Cancer Via Activating the Autophagy/DAPK2/Apoptosis Signaling Cascade
    Article Snippet: .. The Proteome ProfilerTM Human Phospho-RTK Array Kit was used to determine the relative phosphorylation of human receptor tyrosine kinases (R&D Systems, Cat. No. ARY001B, Minneapolis, MN, USA), and the Proteome ProfilerTM Human Phospho-Kinase Array Kit was used to determine the relative levels of human protein kinase phosphorylation (R&D Systems, Cat. No. ARY003C, Minneapolis, MN, USA). .. Cells were seeded into 6 cm dishes and treated with SP-2 (0.5 μM) for 24 h. After the treatment, cells were scraped, washed with PBS, and lysed with TRIzol reagent (Thermo Fisher Scientific, Waltham, MA, USA) to isolate RNA.

    Article Title: 2020 ACVIM Forum On Demand Research Abstract Program
    Article Snippet: .. The Proteome ProfilerTM Human Phospho‐RTK Array Kit (R & D Systems) provided a platform to assess phosphorylation of 42 different RTKs in primary TCC tissue specimens using the available flash frozen tumor specimens and TCC cell lines. ..

    Article Title: Thiosemicarbazones and selected tyrosine kinase inhibitors synergize in pediatric solid tumors: NDRG1 upregulation and impaired prosurvival signaling in neuroblastoma cells.
    Article Snippet: .. The relative levels of phosphorylation of 49 RTKs (Supplementary Figure S1) were assayed using a Proteome ProfilerTM human phospho-RTK array kit (cat. no. ARY001B) purchased from R&D Systems (Minneapolis, MN, United States). ..

    Article Title: Characterization of receptor tyrosine kinase activation and biological activity of toceranib phosphate in canine urothelial carcinoma cell lines
    Article Snippet: .. The Proteome ProfilerTM Human Phospho-RTK Array Kit (R&D Systems, Minneapolis, MN, USA) was used to assess relative phosphorylation of 42 different RTKs in primary UC tumor tissue samples and UC cell lines. ..

    Article Title: Characterization of receptor tyrosine kinase activation and biological activity of toceranib phosphate in canine urothelial carcinoma cell lines
    Article Snippet: .. The Proteome ProfilerTM Human Phospho-RTK Array Kit (R & D Systems) provided a platform to assess phosphorylation of 42 different RTKs in primary UC tumors and UC cell lines. ..

    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). ..



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    proteome profilertm human phospho rtk array kit  (R&D Systems)
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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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    proteome profilertm array human phospho rtk array kit  (R&D Systems)
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    proteome profilertm human phospho rtk antibody arrays  (R&D Systems)
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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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    Average 96 stars, based on 1 article reviews
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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