糖基化

晚期糖基化终末产物和蛋白激酶C对糖尿病大鼠肾脏的影响

Relationship among advanced glycosylation end products , protein kinase C and renal

糖基化终产物对肾间质成纤维细胞DNA损伤的影响

Advanced glycosylation end products induce DNA damage in NRK-49F cells

目的鉴定γB－晶体蛋白非酶糖基化位点。

Objective To identify the glycation sites of lens γ B-crystallin .

能够抑制糖基化终末产物（AGE）的产生，以减少其毒性作用；

Restrain advanced glycation end products ( AGE ) and alleviate toxicity ;

N-烷基嘧啶DNA糖基化酶腺病毒提高人骨肉瘤化疗敏感性的研究

Effect of adenoviral N-methylpurine DNA glycosylase overexpression on chemosensitivity of human osteosarcoma cells

C反应蛋白增加人内皮细胞糖基化终产物受体表达

C Reactive Protein Increases the Expression of Receptor for Advanced Glycation End-products in Human Endothelial Cells

Cthrc1的激活状态是一种锚在细胞膜表面的一种N末端糖基化的三聚体。

And its active form is an N-glycosylated trimer anchored on the cell surface .

序列中有N一糖基化位点，蛋白激酶C磷酸化位点和酪蛋白激酶11磷酸化位点；

The sequence has N-glycosylation site , Protein kinase C phosphorylation site and Casein kinase II phosphorylation site .

目的建立小分子糖基化终产物肽（AGEP）的一种检测方法。

Objective To establish an analyzing approach for low molecular weight advanced glycosylation end products peptide ( AGE P ) .

N糖基化抑制对脑胶质瘤细胞株SWO-38N-GSLs合成的影响

Study on the Effects of N-glycosylation Inhibition on the Expression of N-GSLs in Glioma Cell Line SWO-38

应用糖苷酶酶切和特征性的天冬酰胺序列子的检测发现了39个蛋白中的48个潜在的N型糖基化位点。

Using the characteristic asparagine sequon detection , we found 48 possible N-glycosylation sites in 39 proteins .

它们都含有高百分比的脯氨酸（P）、丝氨酸（S）和苏氨酸（T），含有相当数量的位于胞外区的O-连接糖基化位点。

These predicted G proteins had a relatively high contents of proline , serine , threonine residues and O-linked glycosylation sites .

研究表明：AD脑神经丝蛋白的糖基化修饰水平降低，伴随着磷酸化修饰水平增加，其机制目前尚不清楚。

The study demonstrated that O-Glycosylation of neurofilaments decreased and phosphorylation increased in AD brains .

作者解释道，升高的皮肤晚期糖基化终末产物（AGE）是糖尿病的生物标志物。

An elevated level of skin advanced glycation end products ( AGE ) is a biomarker of diabetes , the authors explain .

竞争性RT-PCR法定量检测糖基化磷脂酰肌醇特异性磷脂酶D基因的表达

Competitive RT - PCR assay for quantification of GPI-PLD gene expression

结论吡哆胺对体外晚期糖基化反应和AGEs形成有明显抑制作用。

Conclusion pyridoxamine displayed significantly inhibitory effect on advanced glycation reaction and AGEs formation in vitro .

结论成功地构建了t－PAcDNA糖基化位点突变体。

CONCLUSIONS The mutants of t-PA cDNA clone at glycosylation sites are successfully constructed .

上述功能的发挥，很大程度上依赖于其胞外区片段（extracellulardomain，ed）的表达及糖基化修饰作用。

The exertion of the function mostly depend on the expression and glycosylation of its extracellular domain .

脑缺血后晚期糖基化终产物受体（RAGE）的表达

Expression of Advanced Glycation Receptor Products ( RAGE ) after Cerebral Ischemia

S蛋白由1256个氨基酸组成，有23个潜在的糖基化位点，其N端和C端相对保守。

SARS-CoV Spike protein , which has 23 pieces larvaceous glycosylation sit , consists of 1256 amino acid . Its N-terminals and C-terminals is corresponding conservative .

黄芪对IgA肾病患者免疫球蛋白分子糖基化异常的调节作用

The Effect of Astragalus Membranaceus on Galactosylation of IgA in IgA Nephropathy Patients

而最近研究发现，晚期糖基化终产物受体（receptorforadvancedglycationendproducts，RAGE）与前列腺癌也密切相关。

Recent studies have found that the receptor for advanced glycation end products ( RAGE ) is closely related to prostate cancer .

先天性Ia型糖基化障碍患者的骨骼发育不良和脊髓病

Skeletal dysplasia and myelopathy in congenital disorder of glycosylation type Ia

结论：糖基化终产物可促进大鼠主动脉平滑肌细胞MMP-2的表达。

Conclusion : Expression of MMP-2 of VSMCs can be promoted by AGEs .

雷公藤内酯醇对IgA肾病大鼠血清IgA异常糖基化的影响

Effects of triptolide on abnormal glycosylation of serum IgA in rats with IgA nephropathy

糖基化低密度脂蛋白增强人外周血单核巨噬细胞的Sis基因表达

Enhancement of sis Gene Expression in Human Monocyte-macrophages by Glycosylated Low Density Lipoprotein

SDS-PAGE结果和FT-IR分析结果均证明了糖基化接枝反应的发生。

The results of SDS-PAGE and infrared analysis proved that the glycosylation grafting reaction happened .

CGMP具有不同的种类，主要是由于其不同的糖基化和磷酸化结构。

CGMP is heterogeneous due to different glycosylation or phosphorylation .

GSH、LA与蛋白糖基化反应体系共育后AGEs含量均显著下降，GSH强于LA的作用，但对体系内羰基含量无明显影响；

AGEs content was significantly decreased after protein glycation system were incubated with GSH and LA for 8 weeks .

PAI－1糖基化位点突变体的构建及其在哺乳动物细胞中表达

Construction of mutant glycosylation sites of PAI-1 and expression in mammalian cells