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Deletion of the neuron-specific protein delta-catenin leads to severe cognitive and synaptic dysfunction.神经元特异性蛋白δ-连环蛋白的缺失会导致严重的认知和突触功能障碍。
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2
Pathways towards and away from Alzheimer's disease.通往和远离阿尔茨海默病的途径。
Nature. 2004 Aug 5;430(7000):631-9. doi: 10.1038/nature02621.
3
The promoter of brain-specific angiogenesis inhibitor 1-associated protein 4 drives developmentally targeted transgene expression mainly in adult cerebral cortex and hippocampus.脑特异性血管生成抑制因子1相关蛋白4的启动子主要在成人大脑皮层和海马体中驱动发育靶向性转基因表达。
FEBS Lett. 2004 May 21;566(1-3):87-94. doi: 10.1016/j.febslet.2004.03.106.
4
Glutamate-induced delta-catenin redistribution and dissociation from postsynaptic receptor complexes.谷氨酸诱导δ-连环蛋白重新分布并从突触后受体复合物中解离。
Neuroscience. 2002;115(4):1009-21. doi: 10.1016/s0306-4522(02)00532-8.
5
Presenilin-1 mutations of leucine 166 equally affect the generation of the Notch and APP intracellular domains independent of their effect on Abeta 42 production.亮氨酸166位点的早老素-1突变同样会影响Notch和APP细胞内结构域的生成，且与其对β淀粉样蛋白42生成的影响无关。
Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8025-30. doi: 10.1073/pnas.112686799. Epub 2002 Jun 4.
6
Dendrite-like process formation and cytoskeletal remodeling regulated by delta-catenin expression.由δ-连环蛋白表达调控的树突状突起形成和细胞骨架重塑。
Exp Cell Res. 2002 May 1;275(2):171-84. doi: 10.1006/excr.2002.5503.
7
A presenilin-1/gamma-secretase cleavage releases the E-cadherin intracellular domain and regulates disassembly of adherens junctions.早老素-1/γ-分泌酶切割可释放E-钙黏蛋白细胞内结构域，并调节黏附连接的解体。
EMBO J. 2002 Apr 15;21(8):1948-56. doi: 10.1093/emboj/21.8.1948.
8
Presenilin-dependent gamma-secretase activity modulates neurite outgrowth.早老素依赖性γ-分泌酶活性调节神经突生长。
Neurobiol Dis. 2002 Feb;9(1):49-60. doi: 10.1006/nbdi.2001.0447.
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Genetics of Alzheimer's disease.阿尔茨海默病的遗传学
Essays Biochem. 1998;33:117-31. doi: 10.1042/bse0330117.
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Isolation of human delta-catenin and its binding specificity with presenilin 1.
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早老素-1抑制δ-连环蛋白诱导的细胞分支，并促进δ-连环蛋白的加工和周转。

Presenilin-1 inhibits delta-catenin-induced cellular branching and promotes delta-catenin processing and turnover.

作者信息

Kim Jin-Sook, Bareiss Sonja, Kim Kyung Keun, Tatum Rodney, Han Jeong-Ran, Jin Yun Hye, Kim Hangun, Lu Qun, Kim Kwonseop

机构信息

The College of Pharmacy, Chonnam National University, Gwangju, Republic of Korea.

出版信息

Biochem Biophys Res Commun. 2006 Dec 29;351(4):903-8. doi: 10.1016/j.bbrc.2006.10.135. Epub 2006 Nov 2.

DOI:10.1016/j.bbrc.2006.10.135
PMID:17097608
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1800877/
Abstract

Although delta-catenin/neural plakophilin-related armadillo protein (NPRAP) was reported to interact with presenilin-1 (PS-1), the effects of PS-1 on delta-catenin have not been established. In this study, we report that overexpression of PS-1 inhibits the delta-catenin-induced dendrite-like morphological changes in NIH 3T3 cells and promotes delta-catenin processing and turnover. The effects of PS-1 on endogenous delta-catenin processing were confirmed in hippocampal neurons overexpressing PS-1, as well as in the transgenic mice expressing the disease-causing mutant PS-1 (M146V). In addition, disease-causing mutant PS-1 (M146V and L286V) enhanced delta-catenin processing, whereas PS-1/gamma-secretase inhibitors could block the formation of processed forms of delta-catenin. Together, our findings suggest that PS-1 can affect delta-catenin-induced morphogenesis possibly through the regulation of its processing and stability.

摘要

尽管据报道δ-连环蛋白/神经斑菲素相关犰狳蛋白（NPRAP）与早老素-1（PS-1）相互作用，但PS-1对δ-连环蛋白的影响尚未明确。在本研究中，我们报告PS-1的过表达抑制了NIH 3T3细胞中δ-连环蛋白诱导的树突样形态变化，并促进了δ-连环蛋白的加工和周转。在过表达PS-1的海马神经元以及表达致病突变体PS-1（M146V）的转基因小鼠中，证实了PS-1对内源性δ-连环蛋白加工的影响。此外，致病突变体PS-1（M146V和L286V）增强了δ-连环蛋白的加工，而PS-1/γ-分泌酶抑制剂可阻断加工形式的δ-连环蛋白的形成。总之，我们的研究结果表明，PS-1可能通过调节其加工和稳定性来影响δ-连环蛋白诱导的形态发生。