Kenneth Michael Humphries

This paper shows that loss of PFKFB2 in cardiac cells leads to electrophysiological instability, including prolonged repolarization and ventricular tachyarrhythmia, linking glycolytic regulation to heart function.

This study shows that hepatocyte MLKL promotes obesity-driven MASLD-HCC through mitochondrial dysfunction and MFN2 suppression, independent of necroptosis.

This study identifies an interaction between APP and PGAM5, showing that APP regulates mitochondrial respiration by modulating Keap1-Nrf2 signaling.

This study investigates the role of PFKFB2 in cardiac metabolic flexibility and glucose utilization, finding that its loss impairs mitochondrial function and affects systemic glucose homeostasis under stress.

The paper investigates synaptic input changes in VTA dopamine neurons of 3xTg-AD mice, finding enhanced excitatory input and reduced inhibition linked to PKC activity.

This study uses a baboon model of sepsis to analyze cardiomyopathy through multimodal techniques, finding distinct transcriptomic and physiological differences between survivors and non-survivors.

The paper identifies and validates a new inhibitor, B2, of PFKFB2 kinase activity through enzymatic assays and metabolic profiling in A-498 cells.

This study shows that loss of cardiac PFKFB2 leads to metabolic, functional, and electrophysiological changes in the heart, including impaired systolic function and altered electrophysiology.