Spotlight on BACE: The secretases as targets for treatment in Alzheimer disease

被引：18

作者：

Dingwall, C ^{[1
]}

机构：

[1] Neurol CEDD, Harlow CM19 5AW, Essex, England

来源：

JOURNAL OF CLINICAL INVESTIGATION | 2001年 / 108卷 / 09期

关键词：

D O I：

10.1172/JCI14402

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

[No abstract available]

引用

页码：1243 / 1246

页数：4

共 49 条

[31] A ROLE FOR ACIDIC RESIDUES IN DI-LEUCINE MOTIF-BASED TARGETING TO THE ENDOCYTIC PATHWAY [J].

POND, L ;

KUHN, LA ;

TEYTON, L ;

SCHUTZE, MP ;

TAINER, JA ;

JACKSON, MR ;

PETERSON, PA .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1995, 270 (34) :19989-19997

[32] Compartmentalization of β-secretase (Asp2) into low-buoyant density, noncaveolar lipid rafts [J].

Riddell, DR ;

Christie, G ;

Hussain, I ;

Dingwall, C .

CURRENT BIOLOGY, 2001, 11 (16) :1288-1293

[33] Fenchylamine sulfonamide inhibitors of amyloid β peptide production by the γ-secretase proteolytic pathway:: Potential small-molecule therapeutic agents for the treatment of Alzheimer's disease [J].

Rishton, GM ;

Retz, DM ;

Tempest, PA ;

Novotny, J ;

Kahn, S ;

Treanor, JJS ;

Lile, JD ;

Citron, M .

JOURNAL OF MEDICINAL CHEMISTRY, 2000, 43 (12) :2297-2299

[34] BACE knockout mice are healthy despite lacking the primary β-secretase activity in brain:: implications for Alzheimer's disease therapeutics [J].

Roberds, SL ;

Anderson, J ;

Basi, G ;

Bienkowski, MJ ;

Branstetter, DG ;

Chen, KS ;

Freedman, SB ;

Frigon, NL ;

Games, D ;

Hu, K ;

Johnson-Wood, K ;

Kappenman, KE ;

Kawabe, TT ;

Kola, I ;

Kuehn, R ;

Lee, M ;

Liu, WQ ;

Motter, R ;

Nichols, NF ;

Power, M ;

Robertson, DW ;

Schenk, D ;

Schoor, M ;

Shopp, GM ;

Shuck, ME ;

Sinha, S ;

Svensson, KA ;

Tatsuno, G ;

Tintrup, H ;

Wijsman, J ;

Wright, S ;

McConlogue, L .

HUMAN MOLECULAR GENETICS, 2001, 10 (12) :1317-1324

[35]

SALMON PD, 1997, PHARM TREATMENT AZHE, P129

[36]

Sandoval Ignacio V., 1994, Trends in Cell Biology, V4, P292, DOI 10.1016/0962-8924(94)90220-8

[37] Secreted amyloid beta-protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease [J].

Scheuner, D ;

Eckman, C ;

Jensen, M ;

Song, X ;

Citron, M ;

Suzuki, N ;

Bird, TD ;

Hardy, J ;

Hutton, M ;

Kukull, W ;

Larson, E ;

LevyLahad, E ;

Viitanen, M ;

Peskind, E ;

Poorkaj, P ;

Schellenberg, G ;

Tanzi, R ;

Wasco, W ;

Lannfelt, L ;

Selkoe, D ;

Younkin, S .

NATURE MEDICINE, 1996, 2 (08) :864-870

[38] Alzheimer's disease: Genes, proteins, and therapy [J].

Selkoe, DJ .

PHYSIOLOGICAL REVIEWS, 2001, 81 (02) :741-766

[39] L-685,458, an aspartyl protease transition state mimic, is a potent inhibitor of amyloid β-protein precursor γ-secretase activity [J].

Shearman, MS ;

Beher, D ;

Clarke, EE ;

Lewis, HD ;

Harrison, T ;

Hunt, P ;

Nadin, A ;

Smith, AL ;

Stevenson, G ;

Castro, JL .

BIOCHEMISTRY, 2000, 39 (30) :8698-8704

[40] The Pro domain of β-secretase does not confer strict zymogen-like properties but does assist proper folding of the protease domain [J].

Shi, XP ;

Chen, E ;

Yin, KC ;

Na, S ;

Garsky, VM ;

Lai, MT ;

Li, YM ;

Platchek, M ;

Sardana, MK ;

Tang, MJ ;

Thiebeau, J ;

Wood, T ;

Shafer, JA ;

Gardell, SJ .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (13) :10366-10373

← 1 2 3 4 5 →