Suppr超能文献

内源性蛋白激酶对突触小泡中VAMP/突触囊泡蛋白的磷酸化作用。

Phosphorylation of VAMP/synaptobrevin in synaptic vesicles by endogenous protein kinases.

作者信息

Nielander H B, Onofri F, Valtorta F, Schiavo G, Montecucco C, Greengard P, Benfenati F

机构信息

Department of Experimental Medicine, University of Roma Tor Vergata, Italy.

出版信息

J Neurochem. 1995 Oct;65(4):1712-20. doi: 10.1046/j.1471-4159.1995.65041712.x.

Abstract

VAMP/synaptobrevin (SYB), an integral membrane protein of small synaptic vesicles, is specifically cleaved by tetanus neurotoxin and botulinum neurotoxins B, D, F, and G is thought to play an important role in the docking and/or fusion of synaptic vesicles with the presynaptic membrane. Potential phosphorylation sites for various kinases are present in SYB sequence. We have studied whether SYB is a substrate for protein kinases that are present in nerve terminals and known to modulate neurotransmitter release. SYB can be phosphorylated within the same vesicle by endogenous Ca2+/calmodulin-dependent protein kinase II (CaMKII) associated with synaptic vesicles. This phosphorylation reaction occurs rapidly and involves serine and threonine residues in the cytoplasmic region of SYB. Similarly to CaMKII, a casein kinase II (CasKII) activity copurifying with synaptic vesicles is able to phosphorylate SYB selectively on serine residues of the cytoplasmic region. This phosphorylation reaction is markedly stimulated by sphingosine, a sphingolipid known to activate CasKII and to inhibit CaMKII and protein kinase C. The results show that SYB is a potential substrate for protein kinases involved in the regulation of neurotransmitter release and open the possibility that phosphorylation of SYB plays a role in modulating the molecular interactions between synaptic vesicles and the presynaptic membrane.

摘要

VAMP/突触小泡蛋白(SYB)是小突触小泡的一种整合膜蛋白,被破伤风神经毒素以及肉毒杆菌神经毒素B、D、F和G特异性切割,被认为在突触小泡与突触前膜的对接和/或融合中起重要作用。SYB序列中存在各种激酶的潜在磷酸化位点。我们研究了SYB是否是存在于神经末梢且已知可调节神经递质释放的蛋白激酶的底物。SYB可在同一小泡内被与突触小泡相关的内源性钙/钙调蛋白依赖性蛋白激酶II(CaMKII)磷酸化。这种磷酸化反应迅速发生,涉及SYB胞质区域的丝氨酸和苏氨酸残基。与CaMKII类似,与突触小泡共纯化的酪蛋白激酶II(CasKII)活性能够选择性地在SYB胞质区域的丝氨酸残基上使其磷酸化。这种磷酸化反应受到鞘氨醇的显著刺激,鞘氨醇是一种已知可激活CasKII并抑制CaMKII和蛋白激酶C的鞘脂。结果表明,SYB是参与神经递质释放调节的蛋白激酶的潜在底物,并开启了SYB磷酸化在调节突触小泡与突触前膜之间分子相互作用中发挥作用的可能性。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验