期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 104, 期 6, 页码 1971-1976出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0603997104
关键词
Alzheimer's disease; genetics; model system
资金
- NCRR NIH HHS [G12 RR003060, RR03060] Funding Source: Medline
- NIA NIH HHS [AG00708, AG11875] Funding Source: Medline
Dominant mutations in the amyloid precursor protein (APP) gene are associated with rare cases of familial Alzheimer's disease; however, the normal functions of APP and related proteins remain unclear. The nematode Caenorhabditis elegans has a single APP-related gene, api-1, that is expressed in multiple tissues. Loss of api-1 disrupts several developmental processes, including molting and morphogenesis, and results in larval lethality. The api-1 lethality can be rescued by neuronal expression of the extracellular domain of APL-1. These data highlight the importance of the extracellular domain of an APP family member and suggest that APL-1 acts noncell-autonomously during development. Overexpression of APL-1 also causes several defects, including a high level of larval lethality. Decreased activity of sel-12, a C elegans homologue of the human gamma-secretase component presenilin 1, partially rescues the lethality associated with APL-1 overexpression, suggesting that SEL-12 activity regulates APL-1 activity either directly or indirectly.
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