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. 2013 Feb 8;6(3):710–720. doi: 10.1242/dmm.011445

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© 2013. 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. 5. — PTEN inactivation leads to the development of thyroid hyperplasia. (A) Comparison of representative thyroids from CAG-Cre-ER^T+/−PTEN^fl/fl mice 6–8 weeks after being injected with corn oil (CON) or tamoxifen (TAM). (B) Representative images of hyperplasia in thyroids dissected from three corn-oil-injected (CON) and three tamoxifen-injected (TAM) mice. (C) Immunofluorescence staining showing PTEN loss in CAG-Cre-ER^T+/−PTEN^fl/fl thyroids. Representative images showing PTEN immunofluorescence of mice injected with corn oil displaying no hyperplasic nodules (CON), mice injected with corn oil displaying hyperplasic nodules (CON-Nodule) or mice injected with tamoxifen (TAM). Arrow indicates PTEN-negative immunofluorescence in hyperplasic module.