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本文引用的文献

1
Clathrin-independent endocytosis: an increasing degree of complexity.网格蛋白非依赖型内吞作用:日益复杂的程度。
Histochem Cell Biol. 2018 Aug;150(2):107-118. doi: 10.1007/s00418-018-1678-5. Epub 2018 May 17.
2
Depression in type 1 diabetes was associated with high levels of circulating galectin-3.1型糖尿病中的抑郁症与循环中半乳糖凝集素-3水平升高有关。
Endocr Connect. 2018 Jun;7(6):819-828. doi: 10.1530/EC-18-0108. Epub 2018 May 14.
3
Galectins at a glance.半乳糖凝集素速览。
J Cell Sci. 2018 May 1;131(9):jcs208884. doi: 10.1242/jcs.208884.
4
Distinct cargo-specific response landscapes underpin the complex and nuanced role of galectin-glycan interactions in clathrin-independent endocytosis.在网格蛋白非依赖型内吞作用中,半乳糖凝集素-聚糖相互作用扮演着复杂而微妙的角色,其特定货物特异性的反应图谱为此提供了基础。
J Biol Chem. 2018 May 11;293(19):7222-7237. doi: 10.1074/jbc.RA118.001802. Epub 2018 Mar 26.
5
Galectin-3 is essential for proper bone cell differentiation and activity, bone remodeling and biomechanical competence in mice.半乳糖凝集素-3 对于小鼠中骨骼细胞的正常分化和活性、骨骼重塑和生物力学性能是必不可少的。
Metabolism. 2018 Jun;83:149-158. doi: 10.1016/j.metabol.2018.02.001. Epub 2018 Feb 9.
6
Serum galectin-3, but not galectin-1, levels are elevated in schizophrenia: implications for the role of inflammation.血清半乳糖凝集素-3(galectin-3)水平升高,但半乳糖凝集素-1(galectin-1)水平正常:提示炎症在精神分裂症中的作用。
Psychopharmacology (Berl). 2017 Oct;234(19):2919-2927. doi: 10.1007/s00213-017-4683-9. Epub 2017 Jul 11.
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Glycolipids and Lectins in Endocytic Uptake Processes.内吞摄取过程中的糖脂和凝集素
J Mol Biol. 2016 Oct 27. doi: 10.1016/j.jmb.2016.10.027.
8
Metabolic flux-driven sialylation alters internalization, recycling, and drug sensitivity of the epidermal growth factor receptor (EGFR) in SW1990 pancreatic cancer cells.代谢通量驱动的唾液酸化改变了SW1990胰腺癌细胞中表皮生长因子受体(EGFR)的内化、再循环和药物敏感性。
Oncotarget. 2016 Oct 11;7(41):66491-66511. doi: 10.18632/oncotarget.11582.
9
Galectin-3 Regulates Atrial Fibrillation Remodeling and Predicts Catheter Ablation Outcomes.半乳糖凝集素-3调节心房颤动重塑并预测导管消融结果。
JACC Basic Transl Sci. 2016 Apr;1(3):143-154. doi: 10.1016/j.jacbts.2016.03.003.
10
Glycosylation-Dependent IFN-γR Partitioning in Lipid and Actin Nanodomains Is Critical for JAK Activation.糖基化依赖性干扰素-γ受体在脂质和肌动蛋白纳米结构域中的分区对JAK激活至关重要。
Cell. 2016 Aug 11;166(4):920-934. doi: 10.1016/j.cell.2016.07.003. Epub 2016 Aug 4.

糖基化和聚糖相互作用可以作为细胞外机制促进网格蛋白非依赖的内吞作用。

Glycosylation and glycan interactions can serve as extracellular machinery facilitating clathrin-independent endocytosis.

机构信息

Cell Biology and Physiology Center, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland.

出版信息

Traffic. 2019 Apr;20(4):295-300. doi: 10.1111/tra.12636. Epub 2019 Feb 28.

DOI:10.1111/tra.12636
PMID:30706592
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6420366/
Abstract

In contrast to clathrin-mediated endocytosis (CME) which is well characterized and understood, little is known about the regulation and machinery underlying clathrin-independent endocytosis (CIE). There is also a wide variation in the requirements each individual CIE cargo has for its internalization. Recent studies have shown that CIE is affected by glycosylation and glycan interactions. We briefly review these studies and explore how these studies mesh with one another. We then discuss what this sensitivity to glycan interactions could indicate for the regulation of CIE. We address the spectrum of responses CIE has been shown to have with respect to changes in glycan interactions and attempt to reconcile disparate observations onto a shared conceptual landscape. We focus on the mechanisms by which cells can alter the glycan interactions at the plasma membrane and propose that glycosylation and glycan interactions could provide cells with a tool box with which cells can manipulate CIE. Altered glycosylation is often associated with a number of diseases and we discuss how under different disease settings, glycosylation-based modulation of CIE could play a role in disease progression.

摘要

与已被充分描述和理解的网格蛋白介导的胞吞作用(CME)相反,人们对网格蛋白非依赖的胞吞作用(CIE)的调控和机制知之甚少。每个 CIE 货物对其内化的要求也存在很大差异。最近的研究表明,CIE 受到糖基化和聚糖相互作用的影响。我们简要回顾了这些研究,并探讨了这些研究如何相互契合。然后,我们讨论了这种对聚糖相互作用的敏感性对 CIE 调控的意义。我们讨论了 CIE 对糖基化相互作用变化所表现出的一系列反应,并试图将不同的观察结果纳入一个共同的概念框架。我们专注于细胞改变质膜上糖基化相互作用的机制,并提出糖基化和聚糖相互作用可以为细胞提供一个工具箱,使细胞能够操纵 CIE。糖基化的改变通常与许多疾病有关,我们讨论了在不同的疾病情况下,基于糖基化的 CIE 调节如何在疾病进展中发挥作用。