Modeling CaMKII in cardiac physiology: from molecule to tissue

Modeling CaMKII in cardiac physiology: from molecule to tissue

Post-translational modification of membrane proteins (e.g., ion channels, receptors) by protein kinases is an essential mechanism for control of excitable cell function. Importantly, loss of temporal and/or spatial control of ion channel post-translational modification is common in congenital and acquired forms of cardiac disease and arrhythmia. The multifunctional Ca(2+)/calmodulin-dependent p...

Computer Modeling in Physiology: From Cell to Tissue - Session Introduction

Over the last two decades there have been tremendous advances with quantitative experimental techniques in physiology and signal transduction. On the cellular level these techniques include the scanning confocal microscopy, single channel recordings from intracellular channels, fluorescent dyes that allow visualization of the spatial and temporal dynamics of second messengers, and bioengineered...

Chasing cardiac physiology and pathology down the CaMKII cascade.

Calcium dynamics is central in cardiac physiology, as the key event leading to the excitation-contraction coupling (ECC) and relaxation processes. The primary function of Ca(2+) in the heart is the control of mechanical activity developed by the myofibril contractile apparatus. This key role of Ca(2+) signaling explains the subtle and critical control of important events of ECC and relaxation, ...

CaMKII in sinoatrial node physiology and dysfunction

The calcium and calmodulin-dependent protein kinase II (CaMKII) is present in sinoatrial node (SAN) pacemaker cells and is required for physiological "fight or flight" SAN beating rate responses. Inhibition of CaMKII in SAN does not affect baseline heart rate, but reduces heart rate increases in response to physiological stress. CaMKII senses intracellular calcium (Ca(2) (+)) changes, oxidation...

Modeling Rhythms: from Physiology to Function