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ADAM10 通过切割盘状结构域受体 1(DDR1)的胞外结构域来控制胶原蛋白信号传导以及细胞在胶原蛋白上的迁移。

ADAM10 controls collagen signaling and cell migration on collagen by shedding the ectodomain of discoidin domain receptor 1 (DDR1).

作者信息

Shitomi Yasuyuki, Thøgersen Ida B, Ito Noriko, Leitinger Birgit, Enghild Jan J, Itoh Yoshifumi

机构信息

Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Oxford OX3 7FY, United Kingdom.

Department of Molecular Biology and Genetics, University of Aarhus, DK-8000 Aarhus C, Denmark.

出版信息

Mol Biol Cell. 2015 Feb 15;26(4):659-73. doi: 10.1091/mbc.E14-10-1463. Epub 2014 Dec 24.

Abstract

Discoidin domain receptor 1 (DDR1) is a receptor tyrosine kinase that binds and transmits signals from various collagens in epithelial cells. However, how DDR1-dependent signaling is regulated has not been understood. Here we report that collagen binding induces ADAM10-dependent ectodomain shedding of DDR1. DDR1 shedding is not a result of an activation of its signaling pathway, since DDR1 mutants defective in signaling were shed in an efficient manner. DDR1 and ADAM10 were found to be in a complex on the cell surface, but shedding did not occur unless collagen bound to DDR1. Using a shedding-resistant DDR1 mutant, we found that ADAM10-dependent DDR1 shedding regulates the half-life of collagen-induced phosphorylation of the receptor. Our data also revealed that ADAM10 plays an important role in regulating DDR1-mediated cell adhesion to achieve efficient cell migration on collagen matrices.

摘要

盘状结构域受体1(DDR1)是一种受体酪氨酸激酶,可结合上皮细胞中的各种胶原蛋白并传递信号。然而,DDR1依赖性信号传导是如何被调节的尚不清楚。在此我们报告,胶原蛋白结合诱导DDR1的ADAM10依赖性胞外域脱落。DDR1脱落不是其信号通路激活的结果,因为信号传导有缺陷的DDR1突变体仍能高效脱落。DDR1和ADAM10在细胞表面形成复合物,但除非胶原蛋白与DDR1结合,否则不会发生脱落。使用抗脱落的DDR1突变体,我们发现ADAM10依赖性DDR1脱落调节受体胶原蛋白诱导的磷酸化的半衰期。我们的数据还表明,ADAM10在调节DDR1介导的细胞黏附中发挥重要作用,以实现细胞在胶原蛋白基质上的高效迁移。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcbc/4325837/02e570edf967/659fig1.jpg

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