Journal: Frontiers in Oncology

Article Title: Crosstalk between protein kinases AKT and ERK1/2 in human lung tumor-derived cell models

doi: 10.3389/fonc.2022.1045521

Figure Lengend Snippet: Determining the efficacy of targeted drugs by phosphorylation of their targets. (A) Capivasertib, an AKT inhibitor, increases the phosphorylation of AKT itself. Capivasertib efficacy is demonstrated by inhibited phosphorylation of GSK3β, a downstream target of AKT. DM – vehicle control (DMSO), CAP – capivasertib, +cis – cisplatin. (B) AKT inhibitor VIII (AKTi) and PI3K inhibitor idelalisib (IDE) reduce AKT phosphorylation in control and cisplatin-treated cells. (C) MEK/ERK signaling inhibitors suppress ERK1/2 phosphorylation in control and cisplatin-treated cells. SEL – selumetinib, SCH – ERK inhibitor SCH772984, TRA – trametinib. Representative Western blots are shown. Coomassie-stained protein gels are presented as loading controls. 6-hour-long exposures to the drugs were used. The concentration of cisplatin was 90 µM, and that of inhibitors was 10 µM except for trametinib and SCH772984 (1 µM).

Article Snippet: The following inhibitors of ERK and AKT signal pathways were used in this study: PI3K inhibitor idelalisib CAL-101 (10 µM; Cayman Chemical, Ann Arbor, MI, USA); Akt inhibitor VIII (10 µM, Merck) and capivasertib AZD5363 (10 µM, Cayman chemical); MEK1/2 inhibitors selumetinib AZD6244 (10 µM, Selleck Chemicals, Houston, TX, USA), trametinib (1 µM, Cayman chemical); ERK inhibitor SCH772984 (1 µM, Cayman chemical); FAK inhibitor PF573228 (10 µM, Merck.).

Techniques: Western Blot, Staining, Concentration Assay

Journal: Frontiers in Oncology

Article Title: Crosstalk between protein kinases AKT and ERK1/2 in human lung tumor-derived cell models

doi: 10.3389/fonc.2022.1045521

Figure Lengend Snippet: Crosstalk with negative feedback between ERK and AKT signaling pathways in human lung cancer-derived cell lines. (A, B) MEK/ERK pathway inhibitor selumetinib enhances AKT phosphorylation in the cell lines tested, control (A) and cisplatin-treated cells (B) . (C) MEK inhibitor trametinib as well as ERK inhibitor SCH772984 increase AKT phosphorylation in control and in cisplatin-treated cells. Representative Western blots are shown. Coomassie-stained protein gels are presented as loading controls. 6-hour-long exposures to the drugs were used. DM – vehicle control (DMSO), SEL – selumetinib (10 µM), +cis – cisplatin (90 µM), TRA – trametinib (1 µM), SCH - SCH772984 (1 µM).

Article Snippet: The following inhibitors of ERK and AKT signal pathways were used in this study: PI3K inhibitor idelalisib CAL-101 (10 µM; Cayman Chemical, Ann Arbor, MI, USA); Akt inhibitor VIII (10 µM, Merck) and capivasertib AZD5363 (10 µM, Cayman chemical); MEK1/2 inhibitors selumetinib AZD6244 (10 µM, Selleck Chemicals, Houston, TX, USA), trametinib (1 µM, Cayman chemical); ERK inhibitor SCH772984 (1 µM, Cayman chemical); FAK inhibitor PF573228 (10 µM, Merck.).

Techniques: Derivative Assay, Western Blot, Staining

Journal: Developmental cell

Article Title: EGFR/Pak Signaling Selectively Regulates Glutamine Deprivation-Induced Macropinocytosis

doi: 10.1016/j.devcel.2019.05.043

Figure Lengend Snippet: KEY RESOURCES TABLE

Article Snippet: SCH772984 , Chemietek , Cat#CT-SCH772.

Techniques: Recombinant, Fluorescence, Reverse Transcription, DC Protein Assay, Stripping Membranes, Transfection, Plasmid Preparation, Negative Control, Software