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. 2012 Oct 31;32(44):15547–15564. doi: 10.1523/JNEUROSCI.0412-12.2012

Figure 11.

Figure 11.

A working model, in conditions of gain of function of Tis21 (A), or loss of function of Tis21 in either Ptch1+/+ (B) or Ptch1+/− context (C). Proliferation, differentiation, and migration out of EGL are referred to GCPs. The gray lines in A refer to data from previous reports (Canzoniere et al., 2004; Farioli-Vecchioli et al., 2007). B, C, In Tis21KO and in Ptch1+/−/Tis21KO mice, the expression of Cxcl3 in GCPs and the migration of GCPs out of EGL decrease. C, In Ptch1+/−/Tis21KO mice, this decrease correlates (dotted line) with the enhancement of medulloblastoma frequency. The defect of migration is rescued in both genotypes by exogenous Cxcl3, which, in Ptch1+/−/Tis21KO mice, reduces the area of cerebellar lesions (C). The dashed line on the left indicates no effect on proliferation relative to controls.