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本文引用的文献

1
Expression of N-Acetylglucosaminyltransferase III Suppresses α2,3-Sialylation, and Its Distinctive Functions in Cell Migration Are Attributed to α2,6-Sialylation Levels.N-乙酰葡糖胺基转移酶III的表达抑制α2,3-唾液酸化，其在细胞迁移中的独特功能归因于α2,6-唾液酸化水平。
J Biol Chem. 2016 Mar 11;291(11):5708-5720. doi: 10.1074/jbc.M115.712836. Epub 2016 Jan 22.
2
Glycomic analysis of gastric carcinoma cells discloses glycans as modulators of RON receptor tyrosine kinase activation in cancer.胃癌细胞的糖组学分析揭示聚糖是癌症中RON受体酪氨酸激酶激活的调节因子。
Biochim Biophys Acta. 2016 Aug;1860(8):1795-808. doi: 10.1016/j.bbagen.2015.12.016. Epub 2015 Dec 22.
3
Glycosylation in cancer: mechanisms and clinical implications.癌症中的糖基化：机制与临床意义。
Nat Rev Cancer. 2015 Sep;15(9):540-55. doi: 10.1038/nrc3982. Epub 2015 Aug 20.
4
Glycosylation-dependent lectin-receptor interactions preserve angiogenesis in anti-VEGF refractory tumors.糖基化依赖的凝集素-受体相互作用可维持抗 VEGF 耐药肿瘤中的血管生成。
Cell. 2014 Feb 13;156(4):744-58. doi: 10.1016/j.cell.2014.01.043.
5
Functional organization of Golgi N- and O-glycosylation pathways involves pH-dependent complex formation that is impaired in cancer cells.高尔基体 N-和 O-糖基化途径的功能组织涉及 pH 依赖性的复合物形成，而这种复合物在癌细胞中受到损害。
J Biol Chem. 2011 Nov 4;286(44):38329-38340. doi: 10.1074/jbc.M111.277681. Epub 2011 Sep 12.

Reciprocal Modulation of Terminal Sialylation and Bisecting N-Glycans: A New Axis of Cancer-Cell Glycome Regulation?

作者信息

Magalhães Ana, Mereiter Stefan, Reis Celso

机构信息

i3S-Instituto de Investigação e Inovação em Saúde, Institute of Molecular Pathology and Immunology, University of Porto-IPATIMUP, Porto, Portugal

i3S-Instituto de Investigação e Inovação em Saúde, Institute of Molecular Pathology and Immunology, University of Porto-IPATIMUP, Porto, Portugal Institute of Biomedical Sciences of Abel Salazar-ICBAS, and.

出版信息

J Biol Chem. 2016 Apr 8;291(15):8308. doi: 10.1074/jbc.L116.722462.

DOI:10.1074/jbc.L116.722462
PMID:27060175
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4825029/
Abstract
摘要