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. 2014 Nov 21;14:857. doi: 10.1186/1471-2407-14-857

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© Jiang et al.; licensee BioMed Central Ltd. 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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ERK1/2 activation is mediated by KRAS in GHM cells. (A) Fold change of NRAS, HRAS and KRAS mRNA after silencing with specific siRNAs in HoMel-A1 and HoMel-L1 cells in comparison to scrambled control siRNA (siNeg). Fold changes are expressed as in Figure 4A. (B, D) Combined (left panels) and individual (right panels) contribution of RAS kinases to ERK1/2 activation in HoMel-A1 and HoMel-L1 cells as assessed by Western blot analysis. Representative images of one of two independent experiments made in biological triplicates are shown. (C, E) Quantification of total ERK1/2-normalized NRAS, HRAS, KRAS and P-ERK1/2 protein levels in individual silencings. Shown are the mean ± s.e. of the two independent experiments.