Huntingtin as an essential integrator of intracellular vesicular trafficking

被引：189

作者：

Caviston, Juliane P. ^{[1
]}

Holzbaur, Erika L. F. ^{[1
]}

机构：

[1] Univ Penn, Sch Med, Dept Physiol, Philadelphia, PA 19104 USA

来源：

TRENDS IN CELL BIOLOGY | 2009年 / 19卷 / 04期

关键词：

DISEASE GENE HOMOLOG; AXONAL-TRANSPORT; NEUROTROPHIC FACTOR; MUTANT HUNTINGTIN; TARGETED DISRUPTION; EMBRYONIC LETHALITY; PROTEIN; NEURONS; BRAIN; PHOSPHORYLATION;

D O I：

10.1016/j.tcb.2009.01.005

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The neurodegenerative disorder Huntington's disease is caused by an expansion in the polyglutamine repeat region of the protein huntingtin. Multiple studies in cellular and animal model systems indicate that this mutation imparts a novel toxic function required for disease pathogenesis. However, the normal function of huntingtin, an essential cellular protein in higher vertebrates, is not yet well understood. Emerging data indicate an important role for wild-type huntingtin in the intracellular transport of vesicles and organelles. Here, we discuss current progress on the role of huntingtin in vesicular trafficking, focusing on the proposal that huntingtin might be a crucial regulator of organelle transport along the cellular cytoskeleton.

引用

页码：147 / 155

页数：9

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