Mutation of the conserved N-terminal cysteine (Cys92) of human presenilin 1 causes increased A beta42 secretion in mammalian cells but impaired Notch/lin-12 signalling in C. elegans.
第一作者:
D M,Zhang
第一单位:
Centre for Research in Neurodegenerative Diseases, Department of Medicine (Neurology), The University Health Network, University of Toronto, Ontario, Canada.
作者:
医学主题词
淀粉样β肽类(Amyloid beta-Peptides);动物(Animals);秀丽新小杆线虫(Caenorhabditis elegans);漂亮新小杆线虫蛋白质类(Caenorhabditis elegans Proteins);半胱氨酸(Cysteine);蠕虫蛋白质类(Helminth Proteins);人类(Humans);膜蛋白质类(Membrane Proteins);突变, 误义(Mutation, Missense);肽碎片(Peptide Fragments);点突变(Point Mutation);早老素1(Presenilin-1);蛋白质结构, 三级(Protein Structure, Tertiary);受体, Notch(Receptors, Notch);信号传导(Signal Transduction)
DOI
10.1097/00001756-200009280-00035
PMID
11043553
发布时间
2019-07-18
- 浏览43
Neuroreport
3227-30页
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