Suppr超能文献

Kv1.2钾通道S1-S2连接区上允许的N-糖基化位点:对连接区二级结构及糖基化对通道功能影响的意义

Allowed N-glycosylation sites on the Kv1.2 potassium channel S1-S2 linker: implications for linker secondary structure and the glycosylation effect on channel function.

作者信息

Zhu Jing, Watanabe Itaru, Poholek Amanda, Koss Matthew, Gomez Barbara, Yan Chaowen, Recio-Pinto Esperanza, Thornhill William B

机构信息

Department of Biological Sciences, Fordham University, Bronx, NY 10458, USA.

出版信息

Biochem J. 2003 Nov 1;375(Pt 3):769-75. doi: 10.1042/BJ20030517.

Abstract

N-glycosylation is a post-translational modification that plays a role in the trafficking and/or function of some membrane proteins. We have shown previously that N-glycosylation affected the function of some Kv1 voltage-gated potassium (K+) channels [Watanabe, Wang, Sutachan, Zhu, Recio-Pinto and Thornhill (2003) J. Physiol. (Cambridge, U.K.) 550, 51-66]. Kv1 channel S1-S2 linkers vary in length but their N-glycosylation sites are at similar relative positions from the S1 or S2 membrane domains. In the present study, by a scanning mutagenesis approach, we determined the allowed N-glycosylation sites on the Kv1.2 S1-S2 linker, which has 39 amino acids, by engineering N-glycosylation sites and assaying for glycosylation, using their sensitivity to glycosidases. The middle section of the linker (54% of linker) was glycosylated at every position, whereas both end sections (46% of linker) near the S1 or S2 membrane domains were not. These findings suggested that the middle section of the S1-S2 linker was accessible to the endoplasmic reticulum glycotransferase at every position and was in the extracellular aqueous phase, and presumably in a flexible conformation. We speculate that the S1-S2 linker is mostly a coiled-loop structure and that the strict relative position of native glycosylation sites on these linkers may be involved in the mechanism underlying the functional effects of glycosylation on some Kv1 K+ channels. The S3-S4 linker, with 16 amino acids and no N-glycosylation site, was not glycosylated when an N-glycosylation site was added. However, an extended linker, with an added N-linked site, was glycosylated, which suggested that the native linker was not glycosylated due to its short length. Thus other ion channels or membrane proteins may also have a high glycosylation potential on a linker but yet have similarly positioned native N-glycosylation sites among isoforms. This may imply that the native position of the N-glycosylation site may be important if the carbohydrate tree plays a role in the folding, stability, trafficking and/or function of the protein.

摘要

N-糖基化是一种翻译后修饰,在某些膜蛋白的运输和/或功能中发挥作用。我们之前已经表明,N-糖基化会影响某些Kv1电压门控钾(K+)通道的功能[渡边、王、苏塔灿、朱、雷西奥-平托和索恩希尔(2003年)《生理学杂志》(英国剑桥)550, 51 - 66]。Kv1通道的S1 - S2连接子长度各异,但其N-糖基化位点相对于S1或S2膜结构域的相对位置相似。在本研究中,通过扫描诱变方法,我们通过设计N-糖基化位点并利用其对糖苷酶的敏感性检测糖基化,确定了具有39个氨基酸的Kv1.2 S1 - S2连接子上允许的N-糖基化位点。连接子的中间部分(占连接子的54%)在每个位置都被糖基化,而靠近S1或S2膜结构域的两端部分(占连接子的46%)则没有。这些发现表明,S1 - S2连接子的中间部分在每个位置都可被内质网糖基转移酶识别,处于细胞外水相中,并且大概处于一种灵活的构象。我们推测S1 - S2连接子大多是一种卷曲环结构,并且这些连接子上天然糖基化位点的严格相对位置可能参与了糖基化对某些Kv1 K+通道功能影响的潜在机制。具有16个氨基酸且无N-糖基化位点的S3 - S4连接子,在添加N-糖基化位点后并未被糖基化。然而,添加了N-连接位点的延长连接子被糖基化了,这表明天然连接子因其长度较短而未被糖基化。因此,其他离子通道或膜蛋白在连接子上可能也具有较高的糖基化潜力,但在同种型之间具有相似位置的天然N-糖基化位点。这可能意味着,如果碳水化合物树在蛋白质的折叠、稳定性、运输和/或功能中发挥作用,N-糖基化位点的天然位置可能很重要。

相似文献

引用本文的文献

本文引用的文献

6
The PSIPRED protein structure prediction server.PSIPRED蛋白质结构预测服务器。
Bioinformatics. 2000 Apr;16(4):404-5. doi: 10.1093/bioinformatics/16.4.404.

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