P0-RafTR mice express the kinase domain of human c-raf-leukemia viral oncogene 1 (Raf Kinase, Raf1)/ER (a tamoxifen inducible human estrogen receptor ligand binding domain) fusion gene under the direction of a modified rat myelin protein zero (Mpz) promoter. Expression of the fusion gene is observed in myelinating Schwann cells. P0 is a glycoprotein located in Schwann cells of the peripheral nervous system. Schwann cells are important for regeneration and restoration of nerve function after injury. Demyelination of Schwann cells has been associated with peripheral neuropathies, neurofibromas, and fibrosarcomas. Tamoxifen administration in carrier mice results in the activation of the RAF kinase-fusion protein in myelinating Schwann cells, followed by severe demyelination within the peripheral nervous system that results in ataxia and impaired motor function. Mice exhibit many of the inflammatory responses important for nerve repair including permeability of the blood nerve barrier and recruitment of macrophages and other inflammatory cells. This phenotype is dose-dependent and reversible upon withdrawal of tamoxifen. Axonal fibers in these mice remain structurally unaffected.

P0-RafTR mice transgenic mice can be used to conditionally activate the ERK pathway is Schwann cells. They may have applications in studies related to cancer and peripheral neuropathies.

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B6;CBA-Tg(Mpz-RAF1/ESR1)A668Ayld/J Frozen Embryo