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桥粒:表皮健康与疾病中细胞信号传导和黏附的调节因子。

Desmosomes: regulators of cellular signaling and adhesion in epidermal health and disease.

作者信息

Johnson Jodi L, Najor Nicole A, Green Kathleen J

机构信息

Department of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611 Department of Dermatology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611.

Department of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611.

出版信息

Cold Spring Harb Perspect Med. 2014 Nov 3;4(11):a015297. doi: 10.1101/cshperspect.a015297.

DOI:10.1101/cshperspect.a015297
PMID:25368015
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4208714/
Abstract

Desmosomes are intercellular junctions that mediate cell-cell adhesion and anchor the intermediate filament network to the plasma membrane, providing mechanical resilience to tissues such as the epidermis and heart. In addition to their critical roles in adhesion, desmosomal proteins are emerging as mediators of cell signaling important for proper cell and tissue functions. In this review we highlight what is known about desmosomal proteins regulating adhesion and signaling in healthy skin-in morphogenesis, differentiation and homeostasis, wound healing, and protection against environmental damage. We also discuss how human diseases that target desmosome molecules directly or interfere indirectly with these mechanical and signaling functions to contribute to pathogenesis.

摘要

桥粒是介导细胞间黏附并将中间丝网络锚定到质膜的细胞间连接,为表皮和心脏等组织提供机械弹性。除了在黏附中的关键作用外,桥粒蛋白正逐渐成为对细胞和组织正常功能至关重要的细胞信号传导介质。在这篇综述中,我们重点介绍了桥粒蛋白在健康皮肤中调节黏附和信号传导方面的已知情况——在形态发生、分化和稳态、伤口愈合以及抵御环境损伤方面。我们还讨论了直接靶向桥粒分子或间接干扰这些机械和信号功能从而导致发病机制的人类疾病。

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本文引用的文献

1
The desmosomal protein desmoglein 1 aids recovery of epidermal differentiation after acute UV light exposure.桥粒蛋白桥粒芯糖蛋白1有助于急性紫外线照射后表皮分化的恢复。
J Invest Dermatol. 2014 Aug;134(8):2154-2162. doi: 10.1038/jid.2014.124. Epub 2014 Mar 4.
2
Desmoglein 1 deficiency results in severe dermatitis, multiple allergies and metabolic wasting.桥粒芯糖蛋白 1 缺乏导致严重的皮炎、多种过敏和代谢消耗。
Nat Genet. 2013 Oct;45(10):1244-1248. doi: 10.1038/ng.2739. Epub 2013 Aug 25.
3
The GEF Bcr activates RhoA/MAL signaling to promote keratinocyte differentiation via desmoglein-1.GEF Bcr 通过激活 RhoA/MAL 信号通路促进桥粒芯糖蛋白 1 介导的角质形成细胞分化。
J Cell Biol. 2013 Aug 19;202(4):653-66. doi: 10.1083/jcb.201304133. Epub 2013 Aug 12.
4
Keratins control intercellular adhesion involving PKC-α-mediated desmoplakin phosphorylation.角蛋白控制细胞间黏附,涉及蛋白激酶 C-α介导的桥粒斑蛋白磷酸化。
J Cell Biol. 2013 May 27;201(5):681-92. doi: 10.1083/jcb.201208162. Epub 2013 May 20.
5
MAPKAP kinase 2 (MK2)-dependent and -independent models of blister formation in pemphigus vulgaris.寻常型天疱疮水疱形成的 MAPKAP kinase 2(MK2)依赖和非依赖模型。
J Invest Dermatol. 2014 Jan;134(1):68-76. doi: 10.1038/jid.2013.224. Epub 2013 Jun 27.
6
Plakoglobin as a regulator of desmocollin gene expression.桥粒斑蛋白作为桥粒芯胶蛋白基因表达的调节因子。
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Cadherin mechanotransduction in tissue remodeling.钙黏蛋白在组织重塑中的机械转导。
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Desmoglein-1/Erbin interaction suppresses ERK activation to support epidermal differentiation.桥粒芯糖蛋白 1/表皮受体酪氨酸激酶相互作用抑制 ERK 激活以支持表皮分化。
J Clin Invest. 2013 Apr;123(4):1556-70. doi: 10.1172/JCI65220. Epub 2013 Mar 25.
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Pemphigus vulgaris autoantibody profiling by proteomic technique.寻常型天疱疮自身抗体的蛋白质组学分析。
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