Notch and presenilins in vertebrates and invertebrates: implications for neuronal development and degeneration

被引：63

作者：

Selkoe, DJ ^{[1
]}

机构：

[1] Harvard Univ, Brigham & Womens Hosp, Sch Med, Ctr Neurol Dis, Boston, MA 02115 USA

来源：

CURRENT OPINION IN NEUROBIOLOGY | 2000年 / 10卷 / 01期

关键词：

D O I：

10.1016/S0959-4388(99)00054-9

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Recent progress in elucidating the biology of Notch and presenilin has revealed a close functional relationship between these two proteins during cell fate determination in worms, flies and humans. Presenilins are required for the putatively intramembranous proteolysis of Notch to release its intracellular domain to the nucleus. This finding establishes a specific biochemical role for presenilins in Notch signaling and interfaces with emerging evidence about how frizzled, disheveled and numerous other genes regulate the highly complex Notch pathway. Advances in understanding Notch and presenilin functions in the differentiation of neurons and non-neural cells have important implications not only for development but also for late-life degenerative disorders such as Alzheimer's disease.

引用

页码：50 / 57

页数：8

共 59 条

[21] Indirect evidence for Delta-dependent intracellular processing of notch in Drosophila embryos [J].

Lecourtois, M ;

Schweisguth, F .

CURRENT BIOLOGY, 1998, 8 (13) :771-774

[22]

Levitan D, 1998, DEVELOPMENT, V125, P3101

[23] FACILITATION OF LIN-12-MEDIATED SIGNALING BY SEL-12, A CAENORHABDITIS-ELEGANS S182 ALZHEIMERS-DISEASE GENE [J].

LEVITAN, D ;

GREENWALD, I .

NATURE, 1995, 377 (6547) :351-354

[24] CANDIDATE GENE FOR THE CHROMOSOME-1 FAMILIAL ALZHEIMERS-DISEASE LOCUS [J].

LEVYLAHAD, E ;

WASCO, W ;

POORKAJ, P ;

ROMANO, DM ;

OSHIMA, J ;

PETTINGELL, WH ;

YU, CE ;

JONDRO, PD ;

SCHMIDT, SD ;

WANG, K ;

CROWLEY, AC ;

FU, YH ;

GUENETTE, SY ;

GALAS, D ;

NEMENS, E ;

WIJSMAN, EM ;

BIRD, TD ;

SCHELLENBERG, GD ;

TANZI, RE .

SCIENCE, 1995, 269 (5226) :973-977

[25] Alagille syndrome is caused by mutations in human Jagged1, which encodes a ligand for Notch1 [J].

Li, LH ;

Krantz, ID ;

Deng, Y ;

Genin, A ;

Banta, AB ;

Collins, CC ;

Qi, M ;

Trask, BJ ;

Kuo, WL ;

Cochran, J ;

Costa, T ;

Pierpont, MEM ;

Rand, EB ;

Piccoli, DA ;

Hood, L ;

Spinner, NB .

NATURE GENETICS, 1997, 16 (03) :243-251

[26] Additional evidence for an eight-transmembrane-domain topology for Caenorhabditis elegans and human presenilins [J].

Li, XJ ;

Greenwald, I .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (12) :7109-7114

[27] Human deltex is a conserved regulator of Notch signalling [J].

Matsuno, K ;

Eastman, D ;

Mitsiades, T ;

Quinn, AM ;

Carcanciu, ML ;

Ordentlich, P ;

Kadesch, T ;

Artavanis-Tsakonas, S .

NATURE GENETICS, 1998, 19 (01) :74-78

[28] Effects of PS1 deficiency on membrane protein trafficking in neurons [J].

Naruse, S ;

Thinakaran, G ;

Luo, JJ ;

Kusiak, JW ;

Tomita, T ;

Iwatsubo, T ;

Qian, XZ ;

Ginty, DD ;

Price, DL ;

Borchelt, DR ;

Wong, PC ;

Sisodia, SS .

NEURON, 1998, 21 (05) :1213-1221

[29] Mutations in the human Jagged1 gene are responsible for Alagille syndrome [J].

Oda, T ;

Elkahloun, AG ;

Pike, BL ;

Okajima, K ;

Krantz, ID ;

Genin, A ;

Piccoli, DA ;

Meltzer, PS ;

Spinner, NB ;

Collins, FS ;

Chandrasekharappa, SC .

NATURE GENETICS, 1997, 16 (03) :235-242

[30]

OLAN S, 1998, NEURON, V20, P611

← 1 2 3 4 5 6 →