ERK5 and the regulation of endothelial cell function

Author:

Roberts Owain Llŷr1,Holmes Katherine2,Müller Jürgen3,Cross Darren A.E.4,Cross Michael J.2

Affiliation:

1. NWCRF Institute, School of Biological Sciences, College of Natural Sciences, Bangor University, Bangor LL57 2UW, U.K.

2. Department of Pharmacology and Therapeutics, School of Biomedical Sciences, University of Liverpool, Liverpool L69 3GE, U.K.

3. Warwick Medical School, Clinical Sciences Research Institute, University of Warwick, Coventry CV4 7AL, U.K.

4. AstraZeneca, Alderley Park, Cheshire SK10 4TG, U.K.

Abstract

ERK5 (extracellular-signal-regulated kinase 5), also termed BMK1 [big MAPK1 (mitogen-activated protein kinase 1)], is the most recently discovered member of the MAPK family. It is expressed in a variety of tissues and is activated by a range of growth factors, cytokines and cellular stresses. Targeted deletion of Erk5 in mice has revealed that the ERK5 signalling cascade is critical for normal cardiovascular development and vascular integrity. In vitro studies have revealed that in endothelial cells, ERK5 is required for preventing apoptosis, mediating shear-stress signalling, regulating hypoxia, tumour angiogenesis and cell migration. This review focuses on our current understanding of the role of ERK5 in regulating endothelial cell function.

Publisher

Portland Press Ltd.

Subject

Biochemistry

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