LIS1:: cellular function of a disease-causing gene

被引：72

作者：

Vallee, RB ^{[1
]}

Tai, CY ^{[1
]}

Faulkner, NE ^{[1
]}

机构：

[1] Univ Massachusetts, Sch Med, Dept Cell Biol, Worcester, MA 01605 USA

来源：

TRENDS IN CELL BIOLOGY | 2001年 / 11卷 / 04期

关键词：

D O I：

10.1016/S0962-8924(01)01956-0

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Brain development is severely defective in children with lissencephaly. The highly organized distribution of neurons within the cerebral cortex is disrupted, a condition that might arise from improper migration of neuronal progenitors to their cortical destinations. Type I lissencephaly results from mutations in the LIS1 gene, which has been implicated in the cytoplasmic dynein and platelet-activating factor pathways. Recent studies have identified roles for the product of LIS1 in nuclear migration, mitotic spindle orientation and chromosome alignment, where it appears to act in concert with cytoplasmic dynein. A unifying hypothesis for the subcellular function of LIS1 is presented.

引用

页码：155 / 160

页数：6

共 36 条

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