Cortazzo M H, Kassis E S, Sproul K A, Schor N F
Department of Pediatrics, University of Pittsburgh, Pennsylvania 15213, USA.
J Neurosci. 1996 Jun 15;16(12):3895-9. doi: 10.1523/JNEUROSCI.16-12-03895.1996.
Prevention by nerve growth factor (NGF) of apoptotic death in neural cells has been variously ascribed to binding of NGF to its low-affinity (p75) or high-affinity (trkA) receptor or to a cooperative interaction between the two. In a series of studies using, in turn, neuroblastoma cell lines that express only p75, mutant NGF species that bind selectively to either p75 or trkA, and a polyclonal antibody that binds to the NGF-binding domain of p75, we demonstrate that NGF binding to p75 is both necessary and sufficient for the abrogation of apoptosis in neuroblastoma cells treated with antimitotic agents.
神经生长因子(NGF)对神经细胞凋亡死亡的预防作用,已被不同地归因于NGF与其低亲和力(p75)或高亲和力(trkA)受体的结合,或两者之间的协同相互作用。在一系列研究中,依次使用仅表达p75的神经母细胞瘤细胞系、选择性结合p75或trkA的突变型NGF物种,以及与p75的NGF结合域结合的多克隆抗体,我们证明,NGF与p75的结合对于抗有丝分裂剂处理的神经母细胞瘤细胞中凋亡的消除既是必要的也是充分的。