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. Author manuscript; available in PMC: 2018 May 1.
Published in final edited form as: Mol Cancer Ther. 2017 Feb 6;16(5):793–804. doi: 10.1158/1535-7163.MCT-16-0677

Figure 5. Acquired resistance to ganetespib results in increased activity and expression of p90RSK and its isoforms in KRAS mutant GR NSCLC cells.

Figure 5

(A) p90RSK activity after ganetespib treatment (48 hours) in C and GR cells was analyzed by immunoblotting using total and phospho-specific pan-p90RSK antibodies as indicated. Actin was included as loading control. (B) Comparative illustration of p90RSK isoform structure indicating key phosphorylation sites required for its activation. (C) Expression of p90RSK isoforms after ganetespib treatment (48 hours) in C and GR cells was assessed by immunoblotting using total isoform specific (RED) and phosphorylation isoform specific (BLACK) antibodies as stated and GAPDH was used as loading control.

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