Translational Medical Research Commons^™

Pyk2 Expression And Localization In Cardiac Mitochondria And Its Role In Mitochondrial Calcium Regulation, Ariele Baggett, Celia Fernandez-Sanz, Sergio De La Fuente, Johannes Hoek, Shey-Shing Sheu

Center for Translational Medicine Posters

TRPM2 is a non-selective cation channel located in the plasma membrane of the cell. Upon activation, the channel opens, allowing calcium to enter into the cytosol of the cell, leading ultimately to the phosphorylation and activation of the enzyme Pyk2 (proline-rich tyrosine kinase 2). Once phosphorylated, Pyk2 translocates from the cytosol to the mitochondria, where it regulates the formation of the pore component of the mitochondrial calcium uniporter (MCU) complex. Consequently, this interaction is a key factor in mitochondrial calcium uptake and therefore mitochondrial bioenergetics.

Gsk3Β-Dependent Phosphorylation Of Cypd And Regulation Of Mptp Opening During Myocardial Infarction, Stephen Hurst, Ludovic Gomez, Shey-Shing Sheu

Center for Translational Medicine Posters

Background

Mitochondrial calcium overload and oxidative stress during ischemia reperfusion (I/R) injury remains a major obstacle during percutaneous coronary intervention after acute myocardial infarction. It often leads to an increased susceptibility for mitochondria permeability transition pore (mPTP) opening leading to cell death. Mitochondrial calcium overload and ROS have been identified as key triggers to open the mPTP for over 30 years, yet the exact mechanism has remained elusive. Additionally, glycogen synthase kinase 3β; (GSK-3β;) is proposed as one of the key molecules that regulate mitochondrial dysfunction and injury during I/R. Indeed inhibition of GSK-3β has been shown to be required …