A5032331281- Cardiac electrophysiology and arrhythmias
- Cardiomyopathy and Myosin Studies
- Ion channel regulation and function
- Cardiovascular Effects of Exercise
- Cardiovascular Function and Risk Factors
- Neuroscience and Neural Engineering
- Adenosine and Purinergic Signaling
- Cardiac Ischemia and Reperfusion
- Mitochondrial Function and Pathology
- Muscle Physiology and Disorders
- Bipolar Disorder and Treatment
- Receptor Mechanisms and Signaling
- Neuroscience and Neuropharmacology Research
- Congenital heart defects research
- Viral Infections and Immunology Research
- Ion Channels and Receptors
- Neuroscience of respiration and sleep
- Antimicrobial Peptides and Activities
- Spondyloarthritis Studies and Treatments
- Hearing, Cochlea, Tinnitus, Genetics
- Advanced Battery Technologies Research
- Pharmacological Effects and Toxicity Studies
- Rheumatoid Arthritis Research and Therapies
- CRISPR and Genetic Engineering
- Venomous Animal Envenomation and Studies
The University of Western Australia
2015-2024
QIMR Berghofer Medical Research Institute
2024
University of Maryland, Baltimore
2012-2020
University of Debrecen
2002-2020
Rutgers, The State University of New Jersey
2013
Innsbruck Medical University
2005
Hungarian Academy of Sciences
2004
ABSTRACT The small, basic, and cysteine-rich antifungal protein PAF is abundantly secreted into the supernatant by β-lactam producer Penicillium chrysogenum . inhibits growth of various important plant zoopathogenic filamentous fungi. Previous studies revealed active internalization induction multifactorial detrimental effects, which finally resulted in morphological changes inhibition target In present study, we offer detailed insights mechanism action give evidence for a programmed cell...
Increased reactive oxygen species (ROS) production and elevated intracellular Ca2+ following cardiac ischemia-reperfusion injury are key mediators of cell death the development hypertrophy. The L-type channel is main route for calcium influx in myocytes. Activation leads to a further increase mitochondrial ROS metabolism. We have previously shown that application peptide derived against alpha-interacting domain (AID) decreases myocardial post reperfusion. Herein, we examine efficacy...
Abstract Ion channels are critical to life and respond rapidly stimuli evoke physiological responses. Calcium influx into heart muscle occurs through the ion conducting α1C subunit (Ca v 1.2) of L-type Ca 2+ channel. Glutathionylation 1.2 results in increased calcium is evident ischemic human heart. However controversy exists as whether direct modification responsible for altered function. We directly assessed function purified proteoliposomes. Truncation C terminus mutation cysteines N...
Genetic mutations in cardiac troponin I (cTnI) are associated with development of hypertrophic cardiomyopathy characterized by myocyte remodelling, disorganization cytoskeletal proteins and altered energy metabolism. The L-type Ca(2+) channel is the main route for calcium influx crucial to excitation contraction. also regulates mitochondrial function heart a functional communication between mitochondria via network. We find that kinetics cTnI-G203S myocytes activation causes significantly...
Abstract Changes in the rate and fidelity of mitochondrial protein synthesis impact metabolic physiological roles mitochondria. Here we explored how environmental stress form a high‐fat diet modulates translation affects lifespan mutant mice with error‐prone ( Mrps12 ep / ) or hyper‐accurate ha ribosomes. Intriguingly, although both mutations are metabolically beneficial reducing body weight, decreasing circulating insulin increasing glucose tolerance during diet, they manifest divergent...
Abstract The “Fight or Flight” response is elicited by extrinsic stress and necessary in many species for survival. involves activation of the β-adrenergic signalling pathway. Surprisingly mechanisms have remained unresolved. Calcium influx through cardiac L-type Ca 2+ channel (Ca v 1.2) absolutely required. Here we identify functionally relevant site PKA phosphorylation on human pore forming α1 subunit using a novel approach. We used cell free system where could assess direct effects...
Abstract Familial hypertrophic cardiomyopathy (FHC) patients are advised to avoid strenuous exercise due increased risk of arrhythmias. Mice expressing the human FHC-causing mutation R403Q in myosin heavy chain gene ( MYH6 ) recapitulate phenotype, including cytoskeletal disarray and arrhythmia susceptibility. Following vivo administration isoproterenol, mutant mice exhibited tachyarrhythmias, poor recovery fatigue. Arrhythmias were attenuated with β-blocker atenolol protein kinase A...
Abstract Background Genomic sequencing in congenital heart disease (CHD) patients often discovers novel genetic variants, which are classified as variants of uncertain significance (VUS). Functional analysis each VUS is required specialised laboratories, to determine whether the causative or not, leading lengthy diagnostic delays. We investigated stem cell cardiac modelling and transcriptomics for purpose variant classification using a GATA4 (p.Arg283Cys) patient with CHD. Methods performed...
Maurocalcine (MCa), a 33 amino acid toxin obtained from scorpion venom, has been shown to interact with the isolated skeletal‐type ryanodine receptor (RyR1) and strongly modify its calcium channel gating. In this study, we explored effects of MCa on RyR1 in situ establish whether functional interaction voltage‐sensing dihydropyridine (DHPR) would ability RyR1. developing skeletal muscle cells addition into external medium induced transient resulting activation inhibited effect agonist...
Significance Hypertrophic cardiomyopathy affects 1:500 of the general population. Current drug therapy is used to manage symptoms in patients. There an unmet need for treatments that can prevent cardiomyopathy. Here we identify biomarkers hypertrophic resulting from causing cardiac troponin I mutation Gly203Ser, and present a safe, nontoxic, preventative approach treatment associated
Hypertrophic cardiomyopathy is an inherited disorder due to mutations in contractile proteins that results a stiff, hypercontractile myocardium. To understand the role of cardiac stiffness disease progression, here we create vitro model hypertrophic utilizing hydrogel technology. Culturing wild-type myocytes on hydrogels with Young's Moduli (stiffness) mimicking myocardium sufficient induce hypermetabolic mitochondrial state versus plated simulating healthy Significantly, these data mirror...
Neuronal nitric oxide synthase (nNOS) is considered a regulator of Cav1.2 L-type Ca2+ channels and downstream cycling in the heart. The commonest view that (NO), generated by nNOS activity cardiomyocytes, reduces currents through channels. This gives rise to diminished release from sarcoplasmic reticulum, finally reduced contractility. Here, we report inhibitor substances significantly increase intracellular transients ventricular cardiomyocytes derived adult mouse rat hearts. consistent...