Prion protein as trans-interacting partner for neurons is involved in neurite outgrowth and neuronal survival

被引：162

作者：

Chen, SZ

Mangé, A

Dong, L

Lehmann, S

Schachner, M

机构：

[1] Univ Hamburg, Zentrum Mol Neurobiol, D-20246 Hamburg, Germany

[2] Inst Genet Humaine, CNRS, UPR 1142, F-34396 Montpellier 5, France

来源：

MOLECULAR AND CELLULAR NEUROSCIENCE | 2003年 / 22卷 / 02期

关键词：

D O I：

10.1016/S1044-7431(02)00014-3

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Many uncertainties remain regarding the physiological function of the prion protein PrP and the consequences of its conversion into the pathological scrapie isoform in prion diseases. Here, we show for the first time that different signal transduction pathways are involved in neurite outgrowth and neuronal survival elicited by PrP in cell culture of primary neurons. These pathways include the nonreceptor Src-related family member p59(Fyn), PI3 kinase/Akt, cAMP-dependent protein kinase A, and MAP kinase. Regulation of Bcl-2 and Bax expression also correlates with the survival effect elicited by PrP. The combined results, along with our observation that PrP carries the recognition molecule-related HNK-1 carbohydrate, argue strongly for a role of the molecule in neural recognition by interacting with yet unknown heterophilic neuronal receptors, as shown by comparison of neurite outgrowth from neurons of PrP-deficient and wild-type mice. (C) 2003 Elsevier Science (USA). All rights reserved.

引用

页码：227 / 233

页数：7

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