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Publication : Defects in sensory nerve numbers and growth in mutant Kit and Steel mice.

First Author  Lourenssen S Year  2000
Journal  Neuroreport Volume  11
Issue  6 Pages  1159-65
PubMed ID  10817584 Mgi Jnum  J:103680
Mgi Id  MGI:3610609 Doi  10.1097/00001756-200004270-00004
Citation  Lourenssen S, et al. (2000) Defects in sensory nerve numbers and growth in mutant Kit and Steel mice. Neuroreport 11(6):1159-65
abstractText  The roles in the nervous system of the receptor tyrosine kinase Kit and its ligand, Steel factor, are unclear. We have now found first, that sensory nerve populations are reduced in mutant Kit and Steel mice, implicating Steel-Kit interactions in neuronal development. Second, sensory axonal regeneration (which occurs independently of nerve growth factor, or NGF) is impaired, while collateral sprouting (NGF dependent) is normal. Therefore, there is a selective involvement of Kit signal transduction pathways in nerve growth; supporting this, in wild-type animals Kit was up-regulated in regenerating, but unchanged in sprouting, sensory neurons. The receptor tyrosine kinase Kit thus contrasts with the receptor tyrosine kinase trkA, which is activated by the sprouting stimulus (NGF) but not by the axonal regeneration signal.
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