igf iir  (R&D Systems)

Journal: bioRxiv

Article Title: Chryseobacterium indologenes mediates resistance to osimertinib by activating the IGF1R pathway in EGFR-mutant lung adenocarcinoma

doi: 10.1101/2025.10.08.681060

Figure Lengend Snippet: (A) Phosphorylation of a panel of 49 RTKs was tested in a RTK array. PC9, HCC827, H1650 and H1975 cells, were treated with osimertinib (50 nM, 25 nM, 5 uM and 5 uM, respectively and C. indologenes PCM (100x dilution) for 24h. (B) Western blot of indicated proteins in PC9 cells treated with osimertinib (50 nM) and PCM (100x dilution) for 24h. (C) CCK-8 cell viability assay following treatment with indicated concentrations of IGF1 and IGF2 in PC9 cells. The assay was performed after 3 days of co-incubation. (D) Western blot of indicated proteins in PC9 cells after cells were treated with osimertinib (50 nM) and IGF1 and IGF2 (100 ng/ml) for 24h. (E) Cell viability assay of PC9 cells with knockdown of IGF1R (siIGF1R), MET (siMET) or both IGF1R and MET (siIGF1R +siMET). Cells were treated with osimertinib with or without C. indologenes PCM. (F) Western blot of indicated proteins in PC9 cells treated with siIGF1R, siMET for 24h. (G) CCK-8 cell viability assay following treatment with indicated concentration of osimertinib (10 nM) and linsitinib in PC9 cells, (H) Drug sensitivity assay was performed after 3 days treatment with osimertinib in siIGF1R-PC9 and siMET-PC9 cells.

Article Snippet: To assess whether IGF1R activation mediates resistance in LACs, cells were treated with recombinant human IGF1 (R&D Systems) or IGF2 (R&D Systems) at 0-100 ng/mL for 3 days in the presence or absence of osimertinib.

Techniques: Phospho-proteomics, Western Blot, CCK-8 Assay, Viability Assay, Incubation, Knockdown, Concentration Assay, Sensitive Assay

Journal: Leukemia

Article Title: A complex interplay of intra- and extracellular factors regulates the outcome of fetal- and adult-derived MLL-rearranged leukemia

doi: 10.1038/s41375-024-02235-5

Figure Lengend Snippet: A , B Viability of THP-1 ( A ) and KOPN-8 ( B ) cells following treatment with IGF2 for 4 days. n = 6. Error bars represent SD. **** p < 0.0001, *** p < 0.001. C Log2 protein abundance of IGF2, IGF2 receptor (IGF2R), and IGF2 binding proteins (IGF2BP1, IGF2BP2, and IGF2BP3) in THP-1 and KOPN-8 cell lines treated with/without IGF2. LFQ label-free quantification. n = 4. D Protein network of commonly induced ‘extracellular’ proteins in the secretome of THP-1 and KOPN-8 treated with IGF2. Edges represent known and predicted protein–protein interactions from STRING and node color indicates the Reactome pathway assignments. E Scatterplot showing the average relative expression difference in the secretome of mouse MLLr/WT fetal LMPPs (x-axis) and in the secretome of THP-1 cells treated with/without IGF2 (y-axis). Red color mark proteins involved in the neutrophil degranulation pathway and the bold borders represent proteins significantly changed (adjusted p-value < 0.05) between IGF2-treated and control THP-1 cells. Mouse and human proteins were mapped by their gene names. F Scatterplot showing the average relative expression difference in the secretome of mouse MLLr/WT fetal LMPPs (x-axis) and in the secretome of KOPN-8 cells treated with/without IGF2 (y-axis). Red color mark proteins involved in the neutrophil degranulation pathway and the bold borders represent proteins significantly changed (adjusted p -value < 0.05) between IGF2-treated and control KOPN-8 cells. Mouse and human proteins were mapped by their gene names. See also Figs. and and Tables and .

Article Snippet: Recombinant mouse or human IGF2 (R&D Systems) was added at 50 or 2000 ng/ml (to mouse cells) and 2000 ng/ml (to human cells).

Techniques: Quantitative Proteomics, Binding Assay, Protein-Protein interactions, Expressing, Control