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Development 124:1313–1322 Sasaki H, Nishizaki Y, Hui C, Nakafuku M, Kondoh H (1999) Regulation of Gli2 and Gli3 activities by an amino-terminal repression domain: implication of Gli2 and Gli3 as primary mediators of Shh signaling. Development 126:3915–3924 Sell S (2004) Stem cell origin of cancer and differentiation therapy. Crit Rev Oncol Hematol 51:1–28 Shanley S, Ratcliffe J, Hockey A, Haan E, Oley C, Ravine D, Martin N, Wicking C, ChenevixTrench G (1994) Nevoid basal cell carcinoma syndrome: review of 118 affected individuals.

Endocrinology 145:3961–3970 Frank-Kamenetsky M, Zhang XM, Bottega S, Guicherit O, Wichterle H, Dudek H, Bumcrot D, Wang FY, Jones S, Shulok J, Rubin LL, Porter JA (2002) Small-molecule modulators of Hedgehog signaling: identification and characterization of Smoothened agonists and antagonists. J Biol 1:10 Furumoto TA, Miura N, Akasaka T, Mizutani-Koseki Y, Sudo H, Fukuda K, Maekawa M, Yuasa S, Fu Y, Moriya H, Taniguchi M, Imai K, Dahl E, Balling R, Pavlova M, Gossler A, Koseki H (1999) Notochord-dependent expression of MFH1 and PAX1 cooperates to maintain the proliferation of sclerotome cells during the vertebral column development.

2000), the relevance of the mutation in vivo remains to be determined. To further investigate the contribution of Tiam1 to the formation and progression of tumors in vivo, Tiam1-deficient mice were generated. As expected, these mice displayed reduced Rac1 activity, and were resistant to the development of Ras-induced skin tumors (Malliri et al. 2002). The few tumors that did develop in Tiam1-null mice exhibited a reduced growth rate compared to Ras-induced tumors in wild-type mice. Furthermore, embryonic fibroblasts isolated from Tiam1-deficient mice had increased apoptotic activity and impaired proliferation, consistent with in vitro studies that implicate Rac1 in tumor formation.

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