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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Hypogonadotropic hypogonadism and peripheral neuropathy in Ebf2-null mice.

Olf/Ebf transcription factors have been implicated in numerous developmental processes, ranging from B-cell development to neuronal differentiation. We describe mice that carry a targeted deletion within the Ebf2 (O/ E3) gene. In Ebf2-null mutants, because of defective migration of gonadotropin releasing hormone-synthesizing neurons, formation of the neuroendocrine axis (which is essential for pubertal development) is impaired, leading to secondary hypogonadism. In addition, Ebf2(-/-) peripheral nerves feature defective axon sorting, hypomyelination, segmental dysmyelination and axonal damage, accompanied by a sharp decrease in motor nerve conduction velocity. Ebf2-null mice reveal a novel genetic cause of hypogonadotropic hypogonadism and peripheral neuropathy in the mouse, disclosing an important role for Ebf2 in neuronal migration and nerve development.[1]

References

  1. Hypogonadotropic hypogonadism and peripheral neuropathy in Ebf2-null mice. Corradi, A., Croci, L., Broccoli, V., Zecchini, S., Previtali, S., Wurst, W., Amadio, S., Maggi, R., Quattrini, A., Consalez, G.G. Development (2003) [Pubmed]
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