The KIF3 motor transports N-cadherin and organizes the developing neuroepithelium
The KIF3 motor transports N-cadherin and organizes the developing neuroepithelium
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DOI：
10.1038/ncb1249
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发表时间：
2005-05-01
影响因子：
21.3
通讯作者：
Hirokawa, N
中科院分区：
文献类型：
--
作者：
Teng, JL;Rai, T;Hirokawa, N
在发育中的大脑中，神经上皮的组织是由神经祖细胞的增殖和细胞-细胞粘附之间的关键平衡维持的。这背后的分子机制在很大程度上仍然是未知的。通过对Kap3基因条件敲除小鼠的分析，我们发现KIF3分子运动复合物对n -钙粘蛋白的高尔基转运对于维持这种平衡至关重要。N-cadherin和β -catenin通过共免疫沉淀与KIF3复合物结合，并在细胞中与KIF3共定位。此外，在kap3缺失的细胞中，n -钙粘蛋白的亚细胞定位被破坏。综上所述，这些结果表明这种分子马达具有潜在的肿瘤抑制活性。
In the developing brain, the organization of the neuroepithelium is maintained by a critical balance between proliferation and cell - cell adhesion of neural progenitor cells. The molecular mechanisms that underlie this are still largely unknown. Here, through analysis of a conditional knockout mouse for the Kap3 gene, we show that post-Golgi transport of N-cadherin by the KIF3 molecular motor complex is crucial for maintaining this balance. N-cadherin and beta-catenin associate with the KIF3 complex by co-immunoprecipitation, and colocalize with KIF3 in cells. Furthermore, in KAP3-deficient cells, the subcellular localization of N-cadherin was disrupted. Taken together, these results suggest a potential tumour-suppressing activity for this molecular motor.