Viral proteins E1B19K and p35 protect sympathetic neurons from cell death induced by NGF deprivation.
Viral proteins E1B19K and p35 protect sympathetic neurons from cell death induced by NGF deprivation.
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DOI：
10.1083/jcb.128.1.201
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发表时间：
1995-01
期刊：
影响因子：
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通讯作者：
Martinou JC
中科院分区：
文献类型：
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作者：
Martinou I;Fernandez PA;Missotten M;White E;Allet B;Sadoul R;Martinou JC
为了研究神经元细胞死亡的分子机制，我们使用了来自上级颈神经节的交感神经元，其在被剥夺神经生长因子时经历程序性细胞死亡。这些神经元已经显微注射含有编码选定蛋白质的cDNA的表达载体，以测试它们对细胞死亡的调节影响。使用这个程序，我们以前已经表明，交感神经元可以保护神经生长因子剥夺的原癌基因Bcl-2。我们现在报道，腺病毒的E1 B19 K蛋白和杆状病毒的p35蛋白也能拯救神经元。其他腺病毒蛋白E1 A和E1 B55 K对神经元存活没有影响。E1 B55 K，已知阻断p53介导的细胞凋亡的增殖细胞，未能拯救交感神经元，这表明p53是不参与神经元死亡诱导的NGF剥夺。E1 B19 K和p35也与阻断淋巴细胞中Bcl-2功能的Bcl-Xs共注射。虽然Bcl-Xs阻断了Bcl- 2拯救神经元的能力，但它对依赖于E1 B19 K或p35表达的存活没有影响。
To study molecular mechanisms underlying neuronal cell death, we have used sympathetic neurons from superior cervical ganglia which undergo programmed cell death when deprived of nerve growth factor. These neurons have been microinjected with expression vectors containing cDNAs encoding selected proteins to test their regulatory influence over cell death. Using this procedure, we have shown previously that sympathetic neurons can be protected from NGF deprivation by the protooncogene Bcl-2. We now report that the E1B19K protein from adenovirus and the p35 protein from baculovirus also rescue neurons. Other adenoviral proteins, E1A and E1B55K, have no effect on neuronal survival. E1B55K, known to block apoptosis mediated by p53 in proliferative cells, failed to rescue sympathetic neurons suggesting that p53 is not involved in neuronal death induced by NGF deprivation. E1B19K and p35 were also coinjected with Bcl-Xs which blocks Bcl-2 function in lymphoid cells. Although Bcl-Xs blocked the ability of Bcl- 2 to rescue neurons, it had no effect on survival that was dependent upon expression of E1B19K or p35.