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. 2009 Jan 15;18(7):1252–1265. doi: 10.1093/hmg/ddp025

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© 2009 The Author(s)

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 1. — Generation of Tsc2^flox/ko;hGFAP-Cre mice. (A) Weight curves of mutant (Tsc2^flox/ko;hGFAP-Cre) mice (red, n = 17) compared with the control (Tsc2^+/flox) mice (blue, n = 15) demonstrating the retarded growth of the mutant animals. (B) A runted mutant, 21-day-old (P21) mouse compared with a control littermate. Note the domed head and splayed feet in the mutant animal. (C) The brain of the mutant mouse (right) was noticeably larger than the control (left). (D) Ventricles in the mutant mouse were dilated (right). (E) Immunoblot analyses of cortical and hippocampal lysates from mutant (‘Cre+’) mice demonstrated a marked decrease of tuberin, slightly decreased levels of hamartin and large increase in pS6 levels compared with the control (‘Cre-’). α-Tubulin was used as the loading control. (F and G) Pax6 and pS6 immunohistochemistry in E15.5 control (F) and mutant (G) mice showed increased activation of mTORC1 in the radial glial cells of the developing cortex. Scale bars, C, 1 mm; F and G, 10 µm.