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