Presenilin and γ-secretase:: structure meets function

被引：40

作者：

Wolfe, MS

机构：

[1] Brigham & Womens Hosp, Ctr Neurol Dis, Boston, MA 02115 USA

[2] Harvard Univ, Sch Med, Boston, MA USA

来源：

JOURNAL OF NEUROCHEMISTRY | 2001年 / 76卷 / 06期

关键词：

D O I：

10.1046/j.1471-4159.2001.00245.x

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：

引用

页码：1615 / 1620

页数：6

共 62 条

[1] Aspartate mutations in presenilin and γ-secretase inhibitors both impair Notch1 proteolysis and nuclear translocation with relative preservation of Notch1 signaling [J].

Berezovska, O ;

Jack, C ;

McLean, P ;

Aster, JC ;

Hicks, C ;

Xia, WM ;

Wolfe, MS ;

Kimberly, WT ;

Weinmaster, G ;

Selkoe, DJ ;

Hyman, BT .

JOURNAL OF NEUROCHEMISTRY, 2000, 75 (02) :583-593

[2] A novel proteolytic cleavage involved in Notch signaling:: The role of the disintegrin-metalloprotease TACE [J].

Brou, C ;

Logeat, F ;

Gupta, N ;

Bessia, C ;

LeBail, O ;

Doedens, JR ;

Cumano, A ;

Roux, P ;

Black, RA ;

Israël, A .

MOLECULAR CELL, 2000, 5 (02) :207-216

[3] Evidence that tumor necrosis factor α converting enzyme is involved in regulated α-secretase cleavage of the Alzheimer amyloid protein precursor [J].

Buxbaum, JD ;

Liu, KN ;

Luo, YX ;

Slack, JL ;

Stocking, KL ;

Peschon, JJ ;

Johnson, RS ;

Castner, BJ ;

Cerretti, DP ;

Black, RA .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (43) :27765-27767

[4] RELEASE OF EXCESS AMYLOID BETA-PROTEIN FROM A MUTANT AMYLOID BETA-PROTEIN PRECURSOR [J].

CAI, XD ;

GOLDE, TE ;

YOUNKIN, SG .

SCIENCE, 1993, 259 (5094) :514-516

[5] The proteolytic fragments of the Alzheimer's disease-associated presenilin-1 form heterodimers and occur as a 100-150-kDa molecular mass complex [J].

Capell, A ;

Grünberg, J ;

Pesold, B ;

Diehlmann, A ;

Citron, M ;

Nixon, R ;

Beyreuther, K ;

Selkoe, DJ ;

Haass, C .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (06) :3205-3211

[6] Presenilin-1 differentially facilitates endoproteolysis of the β-amyloid precursor protein and Notch [J].

Capell, A ;

Steiner, H ;

Romig, H ;

Keck, S ;

Baader, M ;

Grim, MG ;

Baumeister, R ;

Haass, C .

NATURE CELL BIOLOGY, 2000, 2 (04) :205-211

[7] EARLY-ONSET ALZHEIMERS-DISEASE CAUSED BY MUTATIONS AT CODON-717 OF THE BETA-AMYLOID PRECURSOR PROTEIN GENE [J].

CHARTIERHARLIN, MC ;

CRAWFORD, F ;

HOULDEN, H ;

WARREN, A ;

HUGHES, D ;

FIDANI, L ;

GOATE, A ;

ROSSOR, M ;

ROQUES, P ;

HARDY, J ;

MULLAN, M .

NATURE, 1991, 353 (6347) :844-846

[8] EXCESSIVE PRODUCTION OF AMYLOID BETA-PROTEIN BY PERIPHERAL CELLS OF SYMPTOMATIC AND PRESYMPTOMATIC PATIENTS CARRYING THE SWEDISH FAMILIAL ALZHEIMER-DISEASE MUTATION [J].

CITRON, M ;

VIGOPELFREY, C ;

TEPLOW, DB ;

MILLER, C ;

SCHENK, D ;

JOHNSTON, J ;

WINBLAD, B ;

VENIZELOS, N ;

LANNFELT, L ;

SELKOE, DJ .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (25) :11993-11997

[9] Mutant presenilins of Alzheimer's disease increase production of 42-residue amyloid beta-protein in both transfected cells and transgenic mice [J].

Citron, M ;

Westaway, D ;

Xia, WM ;

Carlson, G ;

Diehl, T ;

Levesque, G ;

JohnsonWood, K ;

Lee, M ;

Seubert, P ;

Davis, A ;

Kholodenko, D ;

Motter, R ;

Sherrington, R ;

Perry, B ;

Yao, H ;

Strome, R ;

Lieberburg, I ;

Rommens, J ;

Kim, S ;

Schenk, D ;

Fraser, P ;

Hyslop, PS ;

Selkoe, DJ .

NATURE MEDICINE, 1997, 3 (01) :67-72

[10] MUTATION OF THE BETA-AMYLOID PRECURSOR PROTEIN IN FAMILIAL ALZHEIMERS-DISEASE INCREASES BETA-PROTEIN PRODUCTION [J].

CITRON, M ;

OLTERSDORF, T ;

HAASS, C ;

MCCONLOGUE, L ;

HUNG, AY ;

SEUBERT, P ;

VIGOPELFREY, C ;

LIEBERBURG, I ;

SELKOE, DJ .

NATURE, 1992, 360 (6405) :672-674

← 1 2 3 4 5 6 7 →