Huntington's disease - Exploiting expression

被引：16

作者：

Bates, GP ^{[1
]}

机构：

[1] Univ London Kings Coll, GKT Sch Med, Div Med & Mol Genet, Guys Hosp, London SE1 9RT, England

来源：

NATURE | 2001年 / 413卷 / 6857期

关键词：

D O I：

10.1038/35099656

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Huntington's disease results from defects in the huntingtin protein, but the exact mechanism has been unclear. Researchers now have a better idea, and the knowledge has proved beneficial — for flies at least.

引用

页码：691 / +

页数：3

共 10 条

[1] Insoluble detergent-resistant aggregates form between pathological and nonpathological lengths of polyglutamine in mammalian cells [J].

Kazantsev, A ;

Preisinger, E ;

Dranovsky, A ;

Goldgaber, D ;

Housman, D .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (20) :11404-11409

[2] Decreased expression of striatal signaling genes in a mouse model of Huntington's disease [J].

Luthi-Carter, R ;

Strand, A ;

Peters, NL ;

Solano, SM ;

Hollingsworth, ZR ;

Menon, AS ;

Frey, AS ;

Spektor, BS ;

Penney, EB ;

Schilling, G ;

Ross, CA ;

Borchelt, DR ;

Tapscott, SJ ;

Young, AB ;

Cha, JHJ ;

Olson, JM .

HUMAN MOLECULAR GENETICS, 2000, 9 (09) :1259-1271

[3]

Marks PA, 2001, CLIN CANCER RES, V7, P759

[4] CREB-binding protein sequestration by expanded polyglutamine [J].

McCampbell, A ;

Taylor, JP ;

Taye, AA ;

Robitschek, J ;

Li, M ;

Walcott, J ;

Merry, D ;

Chai, YH ;

Paulson, H ;

Sobue, G ;

Fischbeck, KH .

HUMAN MOLECULAR GENETICS, 2000, 9 (14) :2197-2202

[5] Defect of histone acetyltransferase activity of the nuclear transcriptional coactivator CBP in Rubinstein-Taybi syndrome [J].

Murata, T ;

Kurokawa, R ;

Krones, A ;

Tatsumi, K ;

Ishii, M ;

Taki, T ;

Masuno, M ;

Ohashi, H ;

Yanagisawa, M ;

Rosenfeld, MG ;

Glass, CK ;

Hayashi, Y .

HUMAN MOLECULAR GENETICS, 2001, 10 (10) :1071-1076

[6] SCA17, a novel autosomal dominant cerebellar ataxia caused by an expanded polyglutamine in TATA-binding protein [J].

Nakamura, K ;

Jeong, SY ;

Uchihara, T ;

Anno, M ;

Nagashima, K ;

Nagashima, T ;

Ikeda, S ;

Tsuji, S ;

Kanazawa, I .

HUMAN MOLECULAR GENETICS, 2001, 10 (14) :1441-1448

[7] Interference by Huntingtin and atrophin-1 with CBP-mediated transcription leading to cellular toxicity [J].

Nucifora, FC ;

Sasaki, M ;

Peters, MF ;

Huang, H ;

Cooper, JK ;

Yamada, M ;

Takahashi, H ;

Tsuji, S ;

Troncoso, J ;

Dawson, VL ;

Dawson, TM ;

Ross, CA .

SCIENCE, 2001, 291 (5512) :2423-2428

[8] Self-assembly of polyglutamine-containing huntingtin fragments into amyloid-like fibrils: Implications for Huntington's disease pathology [J].

Scherzinger, E ;

Sittler, A ;

Schweiger, K ;

Heiser, V ;

Lurz, R ;

Hasenbank, R ;

Bates, GP ;

Lehrach, H ;

Wanker, EE .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (08) :4604-4609

[9] Histone deacetylase inhibitors arrest polyglutamine-dependent neurodegeneration in Drosophila [J].

Steffan, JS ;

Bodai, L ;

Pallos, J ;

Poelman, M ;

McCampbell, A ;

Apostol, BL ;

Kazantsev, A ;

Schmidt, E ;

Zhu, YZ ;

Greenwald, M ;

Kurokawa, R ;

Housman, DE ;

Jackson, GR ;

Marsh, JL ;

Thompson, LM .

NATURE, 2001, 413 (6857) :739-743

[10] The Huntington's disease protein interacts with p53 and CREB-binding protein and represses transcription [J].

Steffan, JS ;

Kazantsev, A ;

Spasic-Boskovic, O ;

Greenwald, M ;

Zhu, YZ ;

Gohler, H ;

Wanker, EE ;

Bates, GP ;

Housman, DE ;

Thompson, LM .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (12) :6763-6768

← 1 →