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Publication : Aberrant development of motor axons and neuromuscular synapses in erbB2-deficient mice.

First Author  Lin W Year  2000
Journal  Proc Natl Acad Sci U S A Volume  97
Issue  3 Pages  1299-304
PubMed ID  10655525 Mgi Jnum  J:60191
Mgi Id  MGI:1352956 Doi  10.1073/pnas.97.3.1299
Citation  Lin W, et al. (2000) Aberrant development of motor axons and neuromuscular synapses in erbB2-deficient mice. Proc Natl Acad Sci U S A 97(3):1299-304
abstractText  Receptor tyrosine kinase erbB2, which is activated by neuregulin, is expressed in Schwann and muscle cells in the developing neuromuscular junction (NMJ). In vitro studies have shown that neuregulin promotes the survival and migration of Schwann cells and stimulates acetylcholine receptor gene transcription in cultured muscle cells. These findings suggest an important role for erbB2 in the development of the NMJ. Here we examine erbB2-deficient mice to determine whether erbB2 is required for NMJ development in vivo. Our analysis shows that there are pre- and postsynaptic defects of developing NMJ in erbB2-deficient embryos. The presynaptic defects include defasciculation and degeneration of the motor nerves, and an absence of Schwann cells. The postsynaptic defect features an impairment of junctional folds at the neuromuscular synapse in the mutants. These results demonstrate that erbB2 is essential for in vivo development of the NMJ.
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