CHANNEL FORMATION IN PLANAR LIPID BILAYERS BY A NEUROTOXIC FRAGMENT OF THE BETA-AMYLOID PEPTIDE

被引：108

作者：

MIRZABEKOV, T

LIN, MC

YUAN, WL

MARSHALL, PJ

CARMAN, M

TOMASELLI, K

LIEBERBURG, I

KAGAN, BL

机构：

[1] UNIV CALIF LOS ANGELES,INST NEUROPSYCHIAT,DEPT PSYCHIAT & BEHAV SCI,LOS ANGELES,CA 90024

[2] UNIV CALIF LOS ANGELES,BRAIN RES INST,LOS ANGELES,CA 90024

[3] ATHENA NEUROSCI INC,S SAN FRANCISCO,CA 94080

[4] W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 1994年 / 202卷 / 02期

关键词：

D O I：

10.1006/bbrc.1994.2047

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Alzheimer's disease (AD) pathology is characterized by plaques, tangles, and neuronal cell loss. The main constituent of plaques is beta-amyloid peptide (A beta), a 39-42 residue peptide which has been linked to disruption of calcium homeostasis and neurotoxicity in vitro. We demonstrate that a neurotoxic fragment of A beta, A beta (25-35) spontaneously inserted into planar lipid membranes to form weakly selective, voltage dependent, ion-permeable channels. We suggest that channel formation may be involved in the pathogenesis of AD and that A beta (25-35) may be the active channel forming segment. (C) 1994 Academic Press, Inc

引用

页码：1142 / 1148

页数：7

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