Genomes and Genes
D Brian Foster
Affiliation: Johns Hopkins University
- Redox signaling and protein phosphorylation in mitochondria: progress and prospectsD Brian Foster
Division of Cardiology, Department of Medicine, The Johns Hopkins University School of Medicine, Ross Research Building, Room 847, 720 Rutland Avenue, Baltimore, MD 21205, USA
J Bioenerg Biomembr 41:159-68. 2009....
- The cardiac acetyl-lysine proteomeD Brian Foster
Division of Cardiology, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
PLoS ONE 8:e67513. 2013..New sites suggest a host of potential mechanisms by which excitation-contraction coupling may also be modulated. ..
- Mitochondrial ROMK channel is a molecular component of mitoK(ATP)D Brian Foster
Division of Cardiology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA
Circ Res 111:446-54. 2012..Objective: To use an unbiased proteomic analysis of the mitochondrial inner membrane to identify the mitochondrial K(+) channel underlying mitoK(ATP)...
- Redox regulation of mitochondrial ATP synthase: implications for cardiac resynchronization therapySheng bing Wang
Department of Medicine, Johns Hopkins University, Baltimore, MD 21224, USA
Circ Res 109:750-7. 2011..Our recent studies have revealed that mitochondrial posttranslational modifications (PTM) may contribute to its benefits, motivating the present study of the oxidative regulation of mitochondrial ATP synthase...
- Nitroxyl-mediated disulfide bond formation between cardiac myofilament cysteines enhances contractile functionWei Dong Gao
Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Circ Res 111:1002-11. 2012..Nitroxyl (HNO), the one-electron-reduced form of nitric oxide, enhances cardiac function in a manner that suggests reversible cysteine modifications of the contractile machinery...
- Mitochondrial protein phosphorylation as a regulatory modality: implications for mitochondrial dysfunction in heart failureBRIAN O'ROURKE
Department of Medicine, Division of Cardiology, The Johns Hopkins University, Baltimore, MD 21205 2195, USA
Congest Heart Fail 17:269-82. 2011..The authors review phosphorylation as a mitochondrial regulatory strategy and highlight its possible role in the pathophysiology of cardiac hypertrophy and failure...
- Creatine kinase-mediated improvement of function in failing mouse hearts provides causal evidence the failing heart is energy starvedAshish Gupta
Department of Medicine, Cardiology Division, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
J Clin Invest 122:291-302. 2012..In addition, these data identify CK as a promising therapeutic target for preventing and treating HF and possibly diseases involving energy-dependent dysfunction in other organs with temporally varying energy demands...
- Identification and characterization of a functional mitochondrial angiotensin systemPeter M Abadir
Division of Geriatric Medicine and Gerontology, Biology of Healthy Aging Program, Johns Hopkins University School of Medicine, Baltimore, MD 21224, USA
Proc Natl Acad Sci U S A 108:14849-54. 2011....
- Constitutive HIF-1α expression blunts the beneficial effects of cardiosphere-derived cell therapy in the heart by altering paracrine factor balanceMichael Bonios
Johns Hopkins University, Baltimore, MD 21205, USA
J Cardiovasc Transl Res 4:363-72. 2011..HIF-1α expression in CDCs blunted the beneficial functional effects of CDC transplantation, suggesting that paracrine factor balance may play an important role in cardiac regeneration...
- CAPON modulates cardiac repolarization via neuronal nitric oxide synthase signaling in the heartKuan Cheng Chang
Institute of Molecular Cardiobiology, The Johns Hopkins University, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 105:4477-82. 2008..Our findings provide a rationale for the association of CAPON gene variants with extremes of the QT interval in human populations...
- Is Kir6.1 a subunit of mitoK(ATP)?D Brian Foster
Institute of Molecular Cardiobiology, Division of Cardiology, Johns Hopkins School of Medicine, Baltimore, MD, USA
Biochem Biophys Res Commun 366:649-56. 2008..1D-, 2D-, and native gel analyses were consistent with these assignments. The data suggest it is premature to assign Kir6.1 a role in mitoK(ATP) on the basis of immunoreactivity alone...