Cardiomyocyte physiology. Real-time recording of sarcomere length changes during cardiomyocyte contraction by using IonOptix Myocyte Contractility System.

NLRP3 is moving along the microtubule.  Differentiated THP-1 cells stably expressing Cherry-NLRP3 (red) were stained with TubulinTracker green to label microtubules (green), and Mitotracker Deep Red FM to label mitochondria (magenta). Arrow indicates an NLRP3 particle, and the arrowhead indicates a mitochondrion. Cells were stimulated with nigericin (3 μM). The video corresponds to 105.27 seconds; the width of the movie is 23.3 μm.  Please see the details in this work.

MARK4 and NLRP3 are moving together to the microtubule-organizing centre.  Differentiated THP-1 cells stably expressing Cherry-NLRP3 (red) and GFPMARK4 (green) were stimulated with nigericin. Arrowhead indicates MTOC where MARK4 is accumulated. The video corresponds to 198.366 seconds; the width of the movie is 30.3 μm. Please see the details in this work.

A mechanistic model of how MARK4 regulates microtubule detyrosination and cardiomyocyte contractility after myocardial infarction (MI): After MI, the increased MARK4 kinase activity phosphorylates MAP4 on the polymerized microtubules, and the phosphorylated MAP4 detaches itself from the polymerized microtubules to form oligomerized MAP4 aggregates in the cytosol; the phosphorylation of MAP4 by MARK4 allows access of the microtubule tubulin carboxypeptidase VASH2/SVBP complex to the polymerized microtubules, thereby promoting α-tubulin detyrosination. Please see the details in this work and this review.