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Figure 8


Fig. 8. Overexpression of an APC-independent form of beta-catenin leads to functional bypass of mDia{Delta}N3 inhibition. (A) Myoblasts were co-transfected with a control plasmid (GFP), {Delta}N3+GFP or {Delta}N3+ beta-catenin S37A and TCF activity determined (mean ± s.e.m., n=5, P<0.0046). (B) MyoD expression in cells transfected as in A. Note that {Delta}N3+ beta-catenin S37A transfected cells retain the elongated morphology typical of {Delta}N3 transfectants but are MyoD+. (C) Quantification of MyoD expression in myoblasts transfected with either {Delta}N3+ beta-catenin S37A or {Delta}N3HindIII+ beta-catenin S37A. The degradation-resistant beta-catenin S37A mutant partially reverses the inhibition of MyoD expression mediated by both mDia derivatives. (mean ± s.e.m., **P<0.0002, n=6; *P<0.046, n=3).





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