INDUCTION OF APOPTOSIS BY THE LOW-AFFINITY NGF RECEPTOR
INDUCTION OF APOPTOSIS BY THE LOW-AFFINITY NGF RECEPTOR
复制标题
DOI：
10.1126/science.8332899
复制
发表时间：
1993-07-16
期刊：
影响因子：
56.9
通讯作者：
BREDESEN, DE
中科院分区：
文献类型：
--
作者：
RABIZADEH, S;OH, J;BREDESEN, DE
神经生长因子（NGF）与细胞受体的结合是某些神经细胞存活所必需的。与Trk A不同，Trk A是一种高亲和力的NGF受体，可为存活和分化传递NGF信号，而低亲和力的NGF受体p75NGFR的功能仍不确定。p75NGFR未结合时，表达p75NGFR可组成性诱导神经细胞死亡；而与NGF或单克隆抗体结合可抑制p75NGFR诱导的细胞死亡。因此，p75NGFR的表达可能解释了一些神经细胞依赖NGF存活的原因。这些发现还表明，p75NGFR与包括肿瘤坏死因子受体、Fas （Apo-1）和CD40在内的一个受体超家族的其他成员具有一些功能上的相似性。
Nerve growth factor (NGF) binding to cellular receptors is required for the survival of some neural cells. In contrast to Trk A, the high-affinity NGF receptor that transduces NGF signals for survival and differentiation, the function of the low-affinity NGF receptor, p75NGFR, remains uncertain. Expression of p75NGFR induced neural cell death constitutively when p75NGFR was unbound; binding by NGF or monoclonal antibody, however, inhibited cell death induced by p75NGFR. Thus, expression of p75NGFR may explain the dependence of some neural cells on NGF for survival. These findings also suggest that p75NGFR has some functional similarities to other members of a superfamily of receptors that include tumor necrosis factor receptors, Fas (Apo-1), and CD40.