Atypical PKC, PKCλ/ι, activates β-secretase and increases Aβ 1–40/42 and phospho-tau in mouse brain and isolated neuronal cells, and may link hyperinsulinemia and other aPKC activators to development of pathological and memory abnormalities in Alzheimer's disease

导出原文传递

翻译打印收藏纠错

作者： Mini P. Sajan ^[1] ; Barbara C. Hansen ^[2] ; Margaret G. Higgs ^[3] ; C. Ron Kahn ^[4] ; Ursula Braun ; Michael Leitges ; Collin R. Park ; David M. Diamond ; Robert V. Farese

作者单位： Departments of Psychology, Molecular Pharmacology and Physiology, Center for Preclinical and ^[1] Joslin Research Foundation, Harvard Medical School ^[2] Internal Medicine and Research Services, James A. Haley Veterans Medical Center ^[3] Biotechnology Centre of Oslo ^[4]

关键词 Alzheimer's Aβ Phospho-tau Beta-secretase Atypical PKC PKC-iota/lambda PKM-zeta Insulin Metformin Akt

发布时间 2018-12-11

翻译满意度评价：

准确一般字义偏差语意偏离译文作用小提交

浏览0

Neurobiology of Aging

2018年61卷

225-237页

相似文献

中文期刊
外文期刊
学位论文
会议论文

检索历史清除

Atypical PKC, PKCλ/ι, activates β-secretase and increases Aβ 1–40/42 and phospho-tau in mouse brain and isolated neuronal cells, and may link hyperinsulinemia and other aPKC activators to development of pathological and memory abnormalities in Alzheimer's disease

Neurobiology of Aging

相似文献

Neurobiology of Aging

相关期刊

参考文献：
指定格式：	NoteExpress EndNote RefWorks NoteFirst

检索历史 清除

Atypical PKC, PKCλ/ι, activates β-secretase and increases Aβ 1–40/42 and phospho-tau in mouse brain and isolated neuronal cells, and may link hyperinsulinemia and other aPKC activators to development of pathological and memory abnormalities in Alzheimer's disease

Neurobiology of Aging

相似文献

Neurobiology of Aging

相关期刊

检索历史清除