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血管炎症之旅中的 DUSPs、曲折与转折。

DUSPs, twists and turns in the Journey to Vascular Inflammation.

机构信息

Department of Pharmacology, Yale University School of Medicine, New Haven, CT, USA.

Department of Comparative Medicine, Yale University School of Medicine, New Haven, CT, USA.

出版信息

FEBS J. 2018 May;285(9):1589-1592. doi: 10.1111/febs.14461. Epub 2018 Apr 22.

DOI:10.1111/febs.14461
PMID:29682902
Abstract

The MAPK phosphatase DUSP6/MKP-3 dephosphorylates ERK1 and 2 and negatively regulates ERK-dependent signaling. Hsu et al. now show that DUSP6/MKP-3 is required for the TNF-α-induced upregulation of the endothelial cell adhesion molecule-1 (ICAM-1) and neutrophil infiltration in endothelial cells, and interestingly, this positive role of DUSP6 on the inflammatory process is independent of ERK signaling.

摘要

丝裂原活化蛋白激酶磷酸酶 DUSP6/MKP-3 使 ERK1 和 ERK2 去磷酸化，从而负调控 ERK 依赖的信号转导。Hsu 等人现在表明，DUSP6/MKP-3 对于 TNF-α诱导的内皮细胞黏附分子-1（ICAM-1）上调和中性粒细胞在内皮细胞中的浸润是必需的，有趣的是，DUSP6 在炎症过程中的这种正向作用不依赖于 ERK 信号。

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