Abstract
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. (C) 2000 Lippincott Williams and Wilkins.
| Original language | English |
|---|---|
| Pages (from-to) | 1159-1165 |
| Number of pages | 7 |
| Journal | NeuroReport |
| Volume | 11 |
| Issue number | 6 |
| DOIs | |
| State | Published - 27 Apr 2000 |
Keywords
- Axonal regeneration
- Collateral sprouting
- DRG neurons
- NGF
- Neuron survival
- Steel factor
- Stem cell factor
- Tyrosine kinase
- c-Kit
Fingerprint
Dive into the research topics of 'Defects in sensory nerve numbers and growth in mutant Kit and Steel mice'. Together they form a unique fingerprint.Cite this
- APA
- Author
- BIBTEX
- Harvard
- Standard
- RIS
- Vancouver