Bicket Alex, Coe Imogen R
Department of Biology, York University, Toronto, Canada M3J 1P3.
Department of Biology, York University, Toronto, Canada M3J 1P3 Department of Chemistry and Biology, Ryerson University, Toronto, Canada M5B 2K3
Biosci Rep. 2016 Aug 31;36(4). doi: 10.1042/BSR20160063. Print 2016 Aug.
Human equilibrative nucleoside transporter 1 (hENT1) transports nucleosides and nucleoside analogue drugs across cellular membranes and is necessary for the uptake of many anti-cancer, anti-parasitic and anti-viral drugs. Previous work, and in silico prediction, suggest that hENT1 is glycosylated at Asn(48) in the first extracellular loop of the protein and that glycosylation plays a role in correct localization and function of hENT1. Site-directed mutagenesis of wild-type (wt) hENT1 removed potential glycosylation sites. Constructs (wt 3xFLAG-hENT1, N48Q-3xFLAG-hENT1 or N288Q-3xFLAG-hENT2) were transiently transfected into HEK293 cells and cell lysates were treated with or without peptide-N-glycosidase F (PNGase-F), followed by immunoblotting analysis. Substitution of N48 prevents hENT1 glycosylation, confirming a single N-linked glycosylation site. N48Q-hENT1 protein is found at the plasma membrane in HEK293 cells but at lower levels compared with wt hENT1 based on S-(4-nitrobenzyl)-6-thioinosine (NBTI) binding analysis (wt 3xFLAG-ENT1 Bmax, 41.5±2.9 pmol/mg protein; N48Q-3xFLAG-ENT1 Bmax, 13.5±0.45 pmol/mg protein) and immunofluorescence microscopy. Although present at the membrane, chloroadenosine transport assays suggest that N48Q-hENT1 is non-functional (wt 3xFLAG-ENT1, 170.80±44.01 pmol/mg protein; N48Q-3xFLAG-ENT1, 57.91±17.06 pmol/mg protein; mock-transfected 74.31±19.65 pmol/mg protein). Co-immunoprecipitation analyses suggest that N48Q ENT1 is unable to interact with self or with wt hENT1. Based on these data we propose that glycosylation at N48 is critical for the localization, function and oligomerization of hENT1.
人平衡核苷转运体1(hENT1)可将核苷及核苷类似物药物转运穿过细胞膜,是许多抗癌、抗寄生虫和抗病毒药物摄取所必需的。先前的研究工作以及计算机模拟预测表明,hENT1在该蛋白第一个细胞外环的Asn(48)处发生糖基化,且糖基化在hENT1的正确定位和功能中发挥作用。对野生型(wt)hENT1进行定点诱变可去除潜在的糖基化位点。构建体(wt 3xFLAG-hENT1、N48Q-3xFLAG-hENT1或N288Q-3xFLAG-hENT2)被瞬时转染至HEK293细胞中,细胞裂解物用或不用肽-N-糖苷酶F(PNGase-F)处理,随后进行免疫印迹分析。N48的替换可阻止hENT1糖基化,证实存在单个N-连接糖基化位点。基于S-(4-硝基苄基)-6-硫代肌苷(NBTI)结合分析(wt 3xFLAG-ENT1 Bmax,41.5±2.9 pmol/mg蛋白;N48Q-3xFLAG-ENT1 Bmax,13.5±0.45 pmol/mg蛋白)和免疫荧光显微镜检查,发现N48Q-hENT1蛋白存在于HEK293细胞的质膜上,但与wt hENT1相比水平较低。尽管存在于膜上,但氯腺苷转运试验表明N48Q-hENT1无功能(wt 3xFLAG-ENT1,170.80±44.01 pmol/mg蛋白;N48Q-3xFLAG-ENT1,57.91±17.06 pmol/mg蛋白; mock转染,74.31±19.65 pmol/mg蛋白)。免疫共沉淀分析表明N48Q ENT1无法与自身或wt hENT1相互作用。基于这些数据,我们提出N48处糖基化对于hENT1的定位、功能和寡聚化至关重要。