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. 2011 Apr 18;4(4):548–555. doi: 10.1242/dmm.006874

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© 2011. Published by The Company of Biologists Ltd

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial Share Alike License (http://creativecommons.org/licenses/by-nc-sa/3.0), which permits unrestricted non-commercial use, distribution and reproduction in any medium provided that the original work is properly cited and all further distributions of the work or adaptation are subject to the same Creative Commons License terms.

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Fig. 3. — Elevation of ERK downstream signaling is associated with tumor formation in the bladder and in papilloma formation. Activation of overall ERK-MAPK signaling was examined in the bladders of wild-type (A,B) and UroIICre⁺Fgfr3^+/K644E (C,D) mice, in papilloma of UroIICre⁺Fgfr3^+/K644EK-Ras^G12D/+ mice (E,F), and in bladder tumors of UroIICre⁺H-Ras^Q61L (G,H) and UroIICre⁺β-catenin^exon3/exon3H-Ras^Q61L (I,J) mice by assessing expression of Pea3 (A,C,E,G,I) and pElk1 (B,D,F,H,J). Upregulation of both Pea3 and pElk1 was observed in the bladder of UroIICre⁺Fgfr3^+/K644E mice compared with that of wild-type, and further upregulation was observed in papilloma of UroIICre⁺Fgfr3^+/K644EK-Ras^G12D/+ mice, as well as in bladder tumor models with H-Ras^Q61L mutation. Scale bar: 200 μm.