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Stabilizing the VE-cadherin-catenin complex blocks leukocyte extravasation and vascular permeability.稳定 VE-钙黏蛋白-catenin 复合物可阻断白细胞渗出和血管通透性。
EMBO J. 2011 Aug 19;30(20):4157-70. doi: 10.1038/emboj.2011.304.
2
Cleavage of E-cadherin by ADAM10 mediates epithelial cell sorting downstream of EphB signalling.E-cadherin 的裂解由 ADAM10 介导,介导 EphB 信号下游的上皮细胞分选。
Nat Cell Biol. 2011 Jul 31;13(9):1100-7. doi: 10.1038/ncb2298.
3
Numb controls E-cadherin endocytosis through p120 catenin with aPKC.麻木通过 p120 连环蛋白与 aPKC 控制 E-钙黏蛋白内吞作用。
Mol Biol Cell. 2011 Sep;22(17):3103-19. doi: 10.1091/mbc.E11-03-0274. Epub 2011 Jul 20.
4
p120 catenin is required for normal renal tubulogenesis and glomerulogenesis.连环蛋白对于正常的肾小管发生和肾小球发生是必需的。
Development. 2011 May;138(10):2099-109. doi: 10.1242/dev.056564.
5
Spatial regulation of Dia and Myosin-II by RhoGEF2 controls initiation of E-cadherin endocytosis during epithelial morphogenesis.RhoGEF2 通过调控 Dia 和肌球蛋白-II 的空间分布来控制上皮形态发生过程中 E-钙黏蛋白内吞作用的起始。
Nat Cell Biol. 2011 May;13(5):529-40. doi: 10.1038/ncb2224. Epub 2011 Apr 24.
6
Deletion of p120-catenin results in a tumor microenvironment with inflammation and cancer that establishes it as a tumor suppressor gene.p120 连环蛋白缺失导致具有炎症和癌症的肿瘤微环境,将其确立为肿瘤抑制基因。
Cancer Cell. 2011 Apr 12;19(4):470-83. doi: 10.1016/j.ccr.2011.02.007.
7
Slit-Robo signaling induces malignant transformation through Hakai-mediated E-cadherin degradation during colorectal epithelial cell carcinogenesis.Slit-Robo 信号通过 Hakai 介导的 E-钙黏蛋白降解诱导结直肠上皮细胞癌变中的恶性转化。
Cell Res. 2011 Apr;21(4):609-26. doi: 10.1038/cr.2011.17. Epub 2011 Feb 1.
8
Numb is a negative regulator of HGF dependent cell scattering and Rac1 activation.麻木是 HGF 依赖性细胞散射和 Rac1 激活的负调节剂。
Exp Cell Res. 2011 Feb 15;317(4):539-51. doi: 10.1016/j.yexcr.2010.12.005. Epub 2010 Dec 11.
9
Ubiquitin: same molecule, different degradation pathways.泛素:同一种分子,不同的降解途径。
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10
Anthrax toxins cooperatively inhibit endocytic recycling by the Rab11/Sec15 exocyst.炭疽毒素协同抑制 Rab11/Sec15 外泌体的内吞再循环。
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黏着连接的周转:通过钙黏蛋白的内吞作用、降解和再循环来调节黏附。

Adherens junction turnover: regulating adhesion through cadherin endocytosis, degradation, and recycling.

作者信息

Kowalczyk Andrew P, Nanes Benjamin A

机构信息

Department of Cell Biology, Emory University School of Medicine, 30332, Atlanta, GA, USA,

出版信息

Subcell Biochem. 2012;60:197-222. doi: 10.1007/978-94-007-4186-7_9.

DOI:10.1007/978-94-007-4186-7_9
PMID:22674073
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4074012/
Abstract

Adherens junctions are important mediators of intercellular adhesion, but they are not static structures. They are regularly formed, broken, and rearranged in a variety of situations, requiring changes in the amount of cadherins, the main adhesion molecule in adherens junctions, present at the cell surface. Thus, endocytosis, degradation, and recycling of cadherins are crucial for dynamic regulation of adherens junctions and control of intercellular adhesion. In this chapter, we review the involvement of cadherin endocytosis in development and disease. We discuss the various endocytic pathways available to cadherins, the adaptors involved, and the sorting of internalized cadherin for recycling or lysosomal degradation. In addition, we review the regulatory pathways controlling cadherin endocytosis and degradation, including regulation of cadherin endocytosis by catenins, cadherin ubiquitination, and growth factor receptor signaling pathways. Lastly, we discuss the proteolytic cleavage of cadherins at the plasma membrane.

摘要

黏着连接是细胞间黏附的重要介导物,但它们并非静态结构。在各种情况下,它们会不断地形成、断裂和重新排列,这需要改变细胞表面黏着连接中主要黏附分子钙黏蛋白的数量。因此,钙黏蛋白的内吞作用、降解和再循环对于黏着连接的动态调节和细胞间黏附的控制至关重要。在本章中,我们综述了钙黏蛋白内吞作用在发育和疾病中的作用。我们讨论了钙黏蛋白可用的各种内吞途径、相关衔接蛋白以及内化钙黏蛋白用于再循环或溶酶体降解的分选过程。此外,我们还综述了控制钙黏蛋白内吞作用和降解的调节途径,包括连环蛋白对钙黏蛋白内吞作用 的调节、钙黏蛋白泛素化以及生长因子受体信号通路。最后,我们讨论了质膜上钙黏蛋白的蛋白水解切割。