MK5: A novel regulator of cardiac fibroblast function?

• Published in: IUBMB life 2017-10, Vol.69 (10), p.785-794
• Main Authors: Sahadevan, Pramod, Allen, Bruce G.
• Format: Article
• Language: English
• Subjects: Animals; ERK3; ERK4; fibroblast; Fibroblasts - cytology; Fibroblasts - enzymology; Gene Expression Regulation; Heart; Heart diseases; Heart Ventricles - cytology; Heart Ventricles - enzymology; Humans; Intracellular Signaling Peptides and Proteins - genetics; Intracellular Signaling Peptides and Proteins - metabolism; Isoenzymes - genetics; Isoenzymes - metabolism; MAP kinase; Mice; Mitogen-Activated Protein Kinase 6 - genetics; Mitogen-Activated Protein Kinase 6 - metabolism; MK5; Myocardium - cytology; Myocardium - enzymology; Myocytes, Cardiac - enzymology; Myocytes, Cardiac - metabolism; p38 MAPK; p38 Mitogen-Activated Protein Kinases - genetics; p38 Mitogen-Activated Protein Kinases - metabolism; Protein Domains; Protein-Serine-Threonine Kinases - genetics; Protein-Serine-Threonine Kinases - metabolism; Rodents; Serine; Signal Transduction; Structure-function relationships; Threonine; Ventricular Remodeling - genetics
• ISSN: 1521-6543; 1521-6551
• DOI: 10.1002/iub.1677

MAP kinase‐activated protein kinases (MKs), protein serine/threonine kinases downstream of the MAPKs, regulate a number of biological functions. MK5 was initially identified as a substrate for p38 MAPK but subsequent studies revealed that MK5 activity is regulated by atypical MAPKs ERK3 and ERK4. However, the roles of these MAPKs in activating MK5 remain controversial. The interactome and physiological function of MK5 are just beginning to be understood. Here, we provide an overview of the structure‐function of MK5 including recent progress in determining its role in cardiac structure and function. The cardiac phenotype of MK5 haplodeficient mice, and the effect of reduced MK5 expression on cardiac remodeling, is also discussed. © 2017 IUBMB Life, 69(10):785–794, 2017