Related Experiment Video
Updated: Jun 25, 2026

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
Published on: June 3, 2018
MK5: A novel regulator of cardiac fibroblast function?
Pramod Sahadevan1, Bruce G Allen1,2,3
1Department of Biochemistry and Molecular Medicine, Université de Montréal and Montreal Heart Institute, Montréal, Québec, Canada.
Abstract:
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.
Related Concept Videos
Regulation of Angiogenesis and Blood Supply
Introduction to Fibroblasts
TGF - β Signaling Pathway

