在Fyn基因缺失小鼠的神经元中，神经细胞黏附分子（NCAM）依赖性的神经突生长受到抑制。
NCAM-dependent neurite outgrowth is inhibited in neurons from Fyn-minus mice.
作者信息
Beggs H E, Soriano P, Maness P F
机构信息
Department of Biochemistry, University of North Carolina School of Medicine, Chapel Hill 27599-7260.
出版信息
J Cell Biol. 1994 Nov;127(3):825-33. doi: 10.1083/jcb.127.3.825.
Abstract
Src-related nonreceptor protein tyrosine kinases in nerve growth cones (p59fyn, pp60c-src, and pp62c-yes) are potential intracellular signaling molecules for cell adhesion molecule-directed axonal growth. To determine whether src-related tyrosine kinases mediate NCAM-dependent neurite outgrowth, cultures of cerebellar and sensory neurons from fyn-, src-, and yes- minus mice were analyzed for neurite outgrowth on monolayers of NCAM140-transfected L fibroblasts. NCAM-dependent neurite outgrowth was selectively inhibited in cultures of cerebellar and dorsal root ganglion neurons from fyn-, but not src- or yes- mice. Neurite outgrowth by fyn-, src-, or yes- neurons on untransfected fibroblast monolayers was unaffected, indicating that these kinases do not contribute significantly to axon growth on at least some integrins or other adhesive substrates present on fibroblasts. This study demonstrates that p59fyn is an essential component of the NCAM signaling pathway leading to axonal growth.
摘要
神经生长锥中的Src相关非受体蛋白酪氨酸激酶（p59fyn、pp60c-src和pp62c-yes）是细胞粘附分子导向轴突生长的潜在细胞内信号分子。为了确定Src相关酪氨酸激酶是否介导NCAM依赖性神经突生长，分析了来自fyn-、src-和yes-缺陷小鼠的小脑和感觉神经元培养物在NCAM140转染的L成纤维细胞单层上的神经突生长情况。在来自fyn-缺陷小鼠而非src-或yes-缺陷小鼠的小脑和背根神经节神经元培养物中，NCAM依赖性神经突生长受到选择性抑制。fyn-、src-或yes-缺陷神经元在未转染的成纤维细胞单层上的神经突生长未受影响，这表明这些激酶对至少某些成纤维细胞上存在的整合素或其他粘附底物上的轴突生长没有显著贡献。这项研究表明，p59fyn是导致轴突生长的NCAM信号通路的重要组成部分。
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