Control of neuronal size homeostasis by trophic factor-mediated coupling of protein degradation to protein synthesis.
Control of neuronal size homeostasis by trophic factor-mediated coupling of protein degradation to protein synthesis.
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DOI：
10.1083/jcb.142.5.1313
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发表时间：
1998-09-07
期刊：
影响因子：
--
通讯作者：
Johnson EM
中科院分区：
文献类型：
--
作者：
Franklin JL;Johnson EM
我们证明，神经生长因子夫妇的交感神经元的蛋白质合成率的长寿蛋白质的降解率。抑制蛋白质合成率的一个特定的百分比造成了几乎相等的百分比减少，在长寿命的蛋白质的降解率，表明近1：1耦合之间的两个过程。短寿命蛋白质的降解速率不受抑制蛋白质合成的影响。当蛋白质合成被抑制时，半衰期增加的蛋白质库中包括肌动蛋白和微管蛋白。这两种蛋白质的半衰期为几天，在蛋白质合成完全被抑制的3天内没有降解。其他七种长寿命蛋白质的半衰期被定量，发现当蛋白质合成被完全阻断时，半衰期增加了84-225%。降解-合成偶联保护细胞在合成减少期间免受蛋白质损失。去除NGF后，蛋白质合成速率大大降低，降解与合成之间失去偶联。解偶联导致细胞蛋白质的净损失和体细胞萎缩。我们建议，耦合蛋白质降解的蛋白质合成的速率是一个基本的机制，神经营养因子保持神经元的大小和生长的稳态控制。
We demonstrate that NGF couples the rate of degradation of long-lived proteins in sympathetic neurons to the rate of protein synthesis. Inhibiting protein synthesis rate by a specific percentage caused an almost equivalent percentage reduction in the degradation rate of long-lived proteins, indicating nearly 1:1 coupling between the two processes. The rate of degradation of short-lived proteins was unaffected by suppressing protein synthesis. Included in the pool of proteins that had increased half-lives when protein synthesis was inhibited were actin and tubulin. Both of these proteins, which had half-lives of several days, exhibited no degradation over a 3-d period when protein synthesis was completely suppressed. The half-lives of seven other long-lived proteins were quantified and found to increase by 84–225% when protein synthesis was completely blocked. Degradation–synthesis coupling protected cells from protein loss during periods of decreased synthesis. The rate of protein synthesis greatly decreased and coupling between degradation and synthesis was lost after removal of NGF. Uncoupling resulted in net loss of cellular protein and somatic atrophy. We propose that coupling the rate of protein degradation to that of protein synthesis is a fundamental mechanism by which neurotrophic factors maintain homeostatic control of neuronal size and perhaps growth.
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影响因子：
19
作者：
DESHAIES, RJ
通讯作者：
DESHAIES, RJ
影响因子：
2.9
作者：
EPSTEIN, D;ELIASBISHKO, S;HERSHKO, A
通讯作者：
HERSHKO, A
DOI：
10.1038/newbio232206a0
发表时间：
1971-01-01
期刊：
NATURE-NEW BIOLOGY
影响因子：
--
作者：
HERSHKO, A;MAMONT, P;TOMKINS, GM
通讯作者：
TOMKINS, GM
DOI：
10.1083/jcb.123.5.1207
发表时间：
1993-12
期刊：
The Journal of cell biology
影响因子：
--
作者：
Deckwerth TL;Johnson EM Jr
通讯作者：
Johnson EM Jr
DOI：
10.1083/jcb.127.6.1717
发表时间：
1994-12
期刊：
The Journal of cell biology
影响因子：
--
作者：
Estus S;Zaks WJ;Freeman RS;Gruda M;Bravo R;Johnson EM Jr
通讯作者：
Johnson EM Jr