proteome profiler mouse phospho rtk array kit r d systems cat  (R&D Systems)

Journal: bioRxiv

Article Title: HIWI2 Influences Endosomal Trafficking and Eph Receptor Signaling in Photoreceptor Cells

doi: 10.64898/2026.03.09.710476

Figure Lengend Snippet: A) Si-Control and Si-HIWI2 661W cell lysates were added to Phospho-RTK arrays. Spots are in duplicate and each pair corresponds to a specific Phospho-RTK. i) The top panel corresponds to control, and ii) while the bottom one corresponds to Si-HIWI2 cells. Phospho-Ephs corresponds to the doublet at E and F rows (marked with red box) showing decreased expression after knockdown of HIWI2. B) and C) Western blot analysis and D) and E) quantification of total and phospho form of EphA2 and EphB2 respectively upon knockdown of HIWI2 in 661W cells. The results were quantified and generated by Graph pad prism software. The students’ t-test was used for statistical analysis. Values are means ± SEM, n = 3. *p < 0.05 and **p < 0.01, ***p < 0.001 were considered statistically significant. Original blots for , and , are given in supplementary Fig.S2B, and C.

Article Snippet: Proteins that were altered after HIWI2 silencing were screened using the Phospho-RTK array kit (ARY001B, CST).

Techniques: Control, Expressing, Knockdown, Western Blot, Generated, Software

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

Journal: Cancer Research Communications

Article Title: Novel Syngeneic Cell Lines for Studying High-Risk BRAF V600E -Driven Colorectal Cancer In Vivo

doi: 10.1158/2767-9764.CRC-25-0599

Figure Lengend Snippet: NaJa cells differ in their response to drug treatment. A, Colony formation assay of NaJa cells treated with vemurafenib (V), encorafenib (E), and trametinib (T) at the indicated concentrations for 10 days. Shown is a representative result from three biological replicates. B–D, Quantification of the data shown in A . Data are presented as the mean ± SD and were normalized to the DMSO control ( n = 3). Statistical significance was calculated using one-way ANOVA and Dunnett multiple comparisons test. *, P < 0.05; **, P < 0.01; ****, P < 0.0001. E, Phospho-RTK array of NaJa cells treated with 1 μmol/L vemurafenib (Vem), 0.5 μmol/L encorafenib (Enco), or 50 nmol/L trametinib (Tram) for 5 days. Shown are the log 2 FCs of treated cells versus DMSO control. Array membranes and cell line specific heatmaps are displayed in Supplementary Fig. S7. F, Western blot showing the effect of a 5-day treatment of the NaJa cells on various signaling pathways. G, Western blot and quantification of HER2 and HER3 ( n = 4). Basal EGFR expression was quantified based on data in ( F ), and five additional biological replicates normalized to the internal loading control. Data are presented as the mean ± SD and were normalized to NaJa-F for comparison. Statistical significance was calculated using one-way ANOVA and Tukey multiple comparisons test. *, P < 0.05; **, P < 0.01; ****, P < 0.0001. H, Bulk RNA-seq of NaJa cells treated with 0.5 μmol/L encorafenib for 1 day or 5 days showing upregulation (red) or downregulation (blue) of ERK target genes and the adjusted P value (bubble size).

Article Snippet: From each sample, the recommended amounts (250 μg) of protein were used for the Proteome Profiler Mouse Phospho-RTK Array Kit (ARY0141, R&D systems).

Techniques: Colony Assay, Control, Western Blot, Protein-Protein interactions, Expressing, Comparison, RNA Sequencing