期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 97, 期 3, 页码 1299-1304出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.97.3.1299
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资金
- NCI NIH HHS [CA09370, T32 CA009370] Funding Source: Medline
- NCRR NIH HHS [P41 RR004050] Funding Source: Medline
- NHLBI NIH HHS [F32 HL009756, HL09756] Funding Source: Medline
- NIA NIH HHS [P01 AG010435] Funding Source: Medline
- NICHD NIH HHS [R01 HD034534, HD34534] Funding Source: Medline
- NINDS NIH HHS [R01 NS014718] Funding Source: Medline
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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