Signal Transduction and Intracellular Trafficking by the Interleukin 36 Receptor

被引：25

作者：

Saha, Siddhartha S. ^{[1
]}

Singh, Divyendu ^{[1
]}

Raymond, Ernest L. ^{[2
]}

Ganesan, Rajkumar ^{[2
]}

Caviness, Gary ^{[2
]}

Grimaldi, Christine ^{[2
]}

Woska, Joseph R., Jr. ^{[2
]}

Mennerich, Detlev ^{[2
]}

Brown, Su-Ellen ^{[2
]}

Mbow, M. Lamine ^{[2
]}

Kao, C. Cheng ^{[1
]}

机构：

[1] Indiana Univ, Dept Mol & Cellular Biochem, Bloomington, IN 47401 USA

[2] Boehringer Ingelheim Pharmaceut, Ridgefield, CT 06877 USA

来源：

JOURNAL OF BIOLOGICAL CHEMISTRY | 2015年 / 290卷 / 39期

关键词：

TOLL-LIKE RECEPTOR-3; ENDOCYTOSIS; FAMILY; CLATHRIN; ENDOSOMES; PATHWAY; CELLS; IL-36; TLR3; ACTIVATION;

D O I：

10.1074/jbc.M115.653378

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

Improper signaling of the IL-36 receptor (IL-36R), a member of the IL-1 receptor family, has been associated with various inflammation-associated diseases. However, the requirements for IL-36R signal transduction remain poorly characterized. This work seeks to define the requirements for IL-36R signaling and intracellular trafficking. In the absence of cognate agonists, IL-36R was endocytosed and recycled to the plasma membrane. In the presence of IL-36, IL-36R increased accumulation in LAMP1 + lysosomes. Endocytosis predominantly used a clathrin-mediated pathway, and the accumulation of the IL-36R in lysosomes did not result in increased receptor turnover. The ubiquitin-binding Tollip protein contributed to IL-36R signaling and increased the accumulation of both subunits of the IL-36R.

引用

页码：23997 / 24006

页数：10

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