Deleted in Colorectal Cancer (DCC) encodes a netrin receptor
Deleted in Colorectal Cancer (DCC) encodes a netrin receptor
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DOI：
10.1016/s0092-8674(00)81336-7
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发表时间：
1996-10-18
期刊：
影响因子：
64.5
通讯作者：
TessierLavigne, M
中科院分区：
文献类型：
--
作者：
KeinoMasu, K;Masu, M;TessierLavigne, M
在神经系统中，轴突发育的导向部分由轴突靶细胞分泌的可扩散的化学引诱物介导。Netrin是脊椎动物脊髓中连合轴突的化学引诱剂，但它们产生作用的机制尚不清楚。我们发现，结肠直肠癌（DCC），免疫球蛋白超家族的跨膜蛋白，脊髓连合轴突上表达，并具有netrin-1结合活性。此外，DCC的抗体在体外选择性地阻断连合轴突的netrin-1依赖性生长。这些结果表明，DCC是介导netrin-1对连合轴突的作用的受体或受体的组分，并且它们补充了DCC和netrin同系物在C.线虫和果蝇。
The guidance of developing axons in the nervous system is mediated partly by diffusible chemoattractants secreted by axonal target cells. Netrins are chemoattractants for commissural axons in the vertebrate spinal cord, but the mechanisms through which they produce their effects are unknown. We show that Deleted in Colorectal Cancer (DCC), a transmembrane protein of the immunoglobulin superfamily, is expressed on spinal commissural axons and possesses netrin-1-binding activity. Moreover, an antibody to DCC selectively blocks the netrin-1-dependent outgrowth of commissural axons in vitro. These results indicate that DCC is a receptor or a component of a receptor that mediates the effects of netrin-1 on commissural axons, and they complement genetic evidence for interactions between DCC and netrin homologs in C. elegans and Drosophila.