首页> 美国卫生研究院文献>Proceedings of the National Academy of Sciences of the United States of America >Insulin and insulin-like growth factor II permit nerve growth factor binding and the neurite formation response in cultured human neuroblastoma cells.
【2h】

Insulin and insulin-like growth factor II permit nerve growth factor binding and the neurite formation response in cultured human neuroblastoma cells.

机译:胰岛素和类胰岛素生长因子II可在培养的人成神经细胞瘤细胞中实现神经生长因子结合和神经突形成反应。

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

In serum-free medium, SH-SY5Y human neuroblastoma cells specifically and reversibly lost the capacity to bind 125I-labeled nerve growth factor (NGF) to the high-affinity sites (slow sites) and to respond by neurite outgrowth, unless physiological concentrations of insulin or insulin-like growth factor II were present. In serum-containing medium, anti-insulin antiserum decreased the neurite formation response to NGF, and insulin supplementation increased the number of available NGF slow sites. The low-affinity NGF fast sites are absent from SH-SY5Y cells and did not emerge on treatment with insulin. Insulin potentiated the induction of neurites by NGF in rat pheochromocytoma PC12 cells also. These results implicate a wider role for insulin and its homologs in the nervous system.
机译:在无血清培养基中,SH-SY5Y人成神经细胞瘤细胞特异性可逆地丧失了将125I标记的神经生长因子(NGF)结合到高亲和力部位(缓慢部位)并通过神经突向外生长做出反应的能力,除非生理浓度为存在胰岛素或类胰岛素生长因子II。在含血清的培养基中,抗胰岛素抗血清降低了对NGF的神经突形成反应,而补充胰岛素则增加了可用NGF慢位点的数量。 SH-SY5Y细胞不存在低亲和力的NGF快速位点,并且在用胰岛素治疗时并未出现。胰岛素还增强了大鼠嗜铬细胞瘤PC12细胞中NGF诱导的神经突。这些结果暗示胰岛素及其同系物在神经系统中的作用更大。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号