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

Receptor protein tyrosine phosphatase sigma inhibits axonal regeneration and the rate of axon extension.

Transgenic mice lacking receptor protein tyrosine phophatase-sigma (RPTPsigma), a type IIa receptor protein tyrosine phosphatase, exhibit severe neural developmental deficits. Continued expression of RPTPsigma in the adult suggests that it plays a functional role in the mature nervous system. To determine if RPTPsigma might influence axonal regeneration, the time course of regeneration following facial nerve crush in wild-type and RPTPsigma (-/-) mice was compared. Mice lacking RPTPsigma exhibited an accelerated rate of functional recovery. Immunocytochemical examination of wild-type neurons in cell culture showed RPTPsigma protein in the growth cone. To determine if RPTPsigma affects the ability of a neuron to extend an axon, the rate of axon growth in neuronal cultures derived from wild-type and RPTPsigma (-/-) embryonic mice was compared. RPTPsigma did not affect the rate of axon initiation, but the rate of axon extension is enhanced in neurons obtained from RPTPsigma (-/-) mice. These findings indicate that RPTPsigma slows axon growth via a mechanism intrinsic to the neuron and identify a role for RPTPsigma regulating axonal regeneration by motoneurons.[1]


  1. Receptor protein tyrosine phosphatase sigma inhibits axonal regeneration and the rate of axon extension. Thompson, K.M., Uetani, N., Manitt, C., Elchebly, M., Tremblay, M.L., Kennedy, T.E. Mol. Cell. Neurosci. (2003) [Pubmed]
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