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Genomes and Genes | N H BishopricSummaryAffiliation: University of Miami Country: USA Publications
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Publications
Evolution of the heart from bacteria to manNanette H Bishopric
Department of Molecular and Cellular Pharmacology, University of Miami, Miami, Florida 33101, USA
Ann N Y Acad Sci 1047:13-29. 2005....
Molecular mechanisms of apoptosis in the cardiac myocyteN H Bishopric
Department of Molecular and Cellular Pharmacology, University of Miami School of Medicine, Miami, Florida 33101, USA
Curr Opin Pharmacol 1:141-50. 2001....
Cytoprotection by Jun kinase during nitric oxide-induced cardiac myocyte apoptosisP Andreka
Department of Molecular and Cellular Pharmacology, University of Miami, FL, USA
Circ Res 88:305-12. 2001..Early, transient activation of JNK serves both to delay and to reduce the total extent of apoptosis in cardiac myocytes...
Oxidation of zinc finger transcription factors: physiological consequencesK A Webster
Department of Molecular and Cellular Pharmacology, University of Miami Medical Center, FL 33136, USA
Antioxid Redox Signal 3:535-48. 2001....
Molecular regulation of the endothelin-1 gene by hypoxia. Contributions of hypoxia-inducible factor-1, activator protein-1, GATA-2, AND p300/CBPK Yamashita
Department of Molecular and Cellular Pharmacology, University of Miami Medical Center, Miami, Florida 33149, USA
J Biol Chem 276:12645-53. 2001..The results support essential roles for AP-1, GATA-2, and NF-1 in stabilizing the binding of HIF-1 and promoting recruitment of p300/CBP to the ET-1 hypoxia response complex...
Reperfusion-activated Akt kinase prevents apoptosis in transgenic mouse hearts overexpressing insulin-like growth factor-1K Yamashita
Department of Molecular and Cellular Pharmacology, University of Miami Medical Center, Miami, Florida, USA
Circ Res 88:609-14. 2001..These results demonstrate that Akt phosphorylation during I/R is modulated by IGF-1 and prevents apoptosis in hearts that overexpress the IGF-1 transgene...
Hypoxia-activated apoptosis of cardiac myocytes requires reoxygenation or a pH shift and is independent of p53K A Webster
Department of Molecular and Cellular Pharmacology, University of Miami Medical Center, Florida 33136, USA
J Clin Invest 104:239-52. 1999..We conclude that acidosis, reoxygenation, and reperfusion, but not hypoxia (or ischemia) alone, are strong stimuli for programmed cell death that is substantially independent of p53...
Control of cardiac-specific transcription by p300 through myocyte enhancer factor-2DT I Slepak
Department of Molecular and Cellular Pharmacology, University of Miami, Florida 33101, USA
J Biol Chem 276:7575-85. 2001..These results show that, in the intact cell, p300 interactions with its protein targets are highly selective and that MEF-2D is the preferred channel for p300-mediated transcriptional control in the heart...
Molecular aspects and gene therapy prospects for diastolic failureK A Webster
Department of Molecular and Cellular Pharmacology, University of Miami Medical Center, Florida, USA
Cardiol Clin 18:621-35. 2000..Such techniques may involve modifying the phosphorylation sites in vitro and replacing wild type proteins in the failing heart with the modified forms, again using regulated AAV vectors for gene delivery...
Nitric oxide and promotion of cardiac myocyte apoptosisPeter Andreka
Semmelweis University Faculty of Medicine, 2nd Department of Medicine, Budapest, Hungary
Mol Cell Biochem 263:35-53. 2004..We will also review evidence implicating NO in the pathophysiology of heart failure, in the context of the extensive and sometimes contradictory body of research on NO and cell survival...
BNip3 and signal-specific programmed death in the heartKeith A Webster
Department of Molecular and Cellular Pharmacology, University of Miami Medical Center, 1600 NW 10th Avenue, RMSB 6038, Miami, FL 33136, USA
J Mol Cell Cardiol 38:35-45. 2005..The sequential induction and activation of BNip3 by hypoxia and acidosis provide a molecular basis for the observation that chronic hypoxia at neutral pH does not promote apoptosis or activate caspases in neonatal cardiac myocytes...
Acidosis regulates the stability, hydrophobicity, and activity of the BH3-only protein Bnip3Donna P Frazier
Department of Pharmacology and the Vascular Biology Institute, University of Miami Medical Center, Florida 33136, USA
Antioxid Redox Signal 8:1625-34. 2006..These results demonstrate a pH-sensitive shift in the stability and apparent hydrophobicity of Bnip3 monomers that correlates closely with membrane binding and function...
Redox stress and the contributions of BH3-only proteins to infarctionKeith A Webster
Department of Molecular and Cellular Pharmacology and the Vascular Biology Institute, University of Miami Medical Center, Florida 33395, USA
Antioxid Redox Signal 8:1667-76. 2006..Here we review the evidence for these cell-death pathways and discuss their relevance to ischemic disease and infarction...
PKC-alpha and TAK-1 are intermediates in the activation of c-Jun NH2-terminal kinase by hypoxia-reoxygenationDonna P Frazier
Department of Molecular and Cellular Pharmacology, Vascular Biology Institute, University of Miami School of Medicine, Miami, Florida 33136, USA
Am J Physiol Heart Circ Physiol 292:H1675-84. 2007..These results identify two new components, PKC and TAK-1, that have not been previously described in this signaling pathway...
Regulation of Bnip3 death pathways by calcium, phosphorylation, and hypoxia-reoxygenationRegina M Graham
Department of Molecular and Cellular Pharmacology and the Vascular Biology Institute, University of Miami School of Medicine, Miami, Florida 33136, USA
Antioxid Redox Signal 9:1309-15. 2007..Elevated levels of the phosphoprotein correlated with initiation of Bnip3-dependent death, whereas the dephosphorylated species correlated with extreme acidosis...
A unique pathway of cardiac myocyte death caused by hypoxia-acidosisRegina M Graham
Department of Molecular and Cellular Pharmacology and the Vascular Biology Institute, University of Miami Medical Center, Miami, FL 33101, USA
J Exp Biol 207:3189-200. 2004..The article also contains new evidence that chronic hypoxia at neutral pH does not promote apoptosis or activate caspases in neonatal cardiac myocytes...
Apoptosis inhibitors for heart diseaseKeith A Webster
Department of Molecular and Cellular Pharmacology, University of Miami Medical Center, 1600 NW 10th Avenue, RMSB 6038, Miami, Fla 33136, USA
Circulation 108:2954-6. 2003
Quantitative control of adaptive cardiac hypertrophy by acetyltransferase p300Jian Qin Wei
University of Miami School of Medicine, Department of Molecular and Cellular Pharmacology, Miami, FL, USA
Circulation 118:934-46. 2008..However, the importance of p300 in the modulation of cardiac growth in vivo is unknown...
Transplantation of stem cells to the heart:Robert J Myerburg
J Cardiovasc Electrophysiol 14:849-50. 2003
Hypoxia and acidosis activate cardiac myocyte death through the Bcl-2 family protein BNIP3Lori A Kubasiak
Department of Molecular and Cellular Pharmacology, University of Miami Medical Center, Miami, FL 33136, USA
Proc Natl Acad Sci U S A 99:12825-30. 2002..Overexpression of wild-type BNIP3, but not a translocation-defective mutant, activated cardiac myocyte death only when the myocytes were acidic. This pathway may figure significantly in muscle loss during myocardial ischemia...
Angiotensin signaling and apoptosis in the neonatal heart: necessary evils?Nanette H Bishopric
Department of Molecular and Cellular Pharmacology, University of Miami School of Medicine, PO Box 016189 R 189, Miami, FL 33101, USA
Pediatr Res 52:322-4. 2002
Activation of c-Jun N-terminal kinase promotes survival of cardiac myocytes after oxidative stressChristopher J Dougherty
Department of Molecular and Cellular Pharmacology, University of Miami Medical Center, 1600 NW 10th Avenue, RMSB 6038, Miami, FL 33136, U.S.A
Biochem J 362:561-71. 2002..The results suggest that JNK activation is protective and that the pathway is largely independent of p38 MAPK or secreted TNFalpha...
Mesenchymal stem cell-derived IL-10 and recovery from infarction: a third pitch for the chordNanette H Bishopric
Circ Res 103:125-7. 2008
Neuroprotective antioxidant STAZN protects against myocardial ischemia/reperfusion injuryJames J Ley
Department of Neurology, University of Miami, Miller School of Medicine, Miami, FL 33101, United States
Biochem Pharmacol 75:448-56. 2008....
Jun kinase delays caspase-9 activation by interaction with the apoptosomeThanh H Tran
Department of Molecular and Cellular Pharmacology, University of Miami Miller School of Medicine, Miami, FL 33136, USA
J Biol Chem 282:20340-50. 2007..We propose that this interaction delays formation of the active apoptosome, promoting cell survival during short bursts of oxidative stress...
Whole blood RNA offers a rapid, comprehensive approach to genetic diagnosis of cardiovascular diseasesTodd E Miller
Department of Medicine, Division of Cardiology, Miller School of Medicine, University of Miami, Miami, Florida 33101, USA
Genet Med 9:23-33. 2007..Genetic testing for these disorders is labor-intensive and expensive. We sought to develop a more rapid, comprehensive, and cost-effective approach...
Bucindolol displays intrinsic sympathomimetic activity in human myocardiumPeter Andreka
Department of Molecular and Cellular Pharmacology, University of Miami School of Medicine, Miami, FL 33101, USA
Circulation 105:2429-34. 2002..Bucindolol has partial agonist properties in rat myocardium, but whether it has agonist activity in human heart is controversial. To address this, we measured the ability of bucindolol to increase cAMP accumulation in human myocardium...
A thousand times NONanette H Bishopric
J Mol Cell Cardiol 34:601-6. 2002
Preventing apoptosis with thioredoxin: ASK me howNanette H Bishopric
Circ Res 90:1237-9. 2002
Gene and cell therapy for heart diseaseRegina M Graham
Department of Molecular and Cellular Pharmacology, University of Miami Medical Center, Florida 33136, USA
IUBMB Life 54:59-66. 2002....
Reversible connexin 43 dephosphorylation during hypoxia and reoxygenation is linked to cellular ATP levelsMark S Turner
Department of Molecular and Cellular Pharmacology, University of Miami, Fla, USA
Circ Res 95:726-33. 2004..The role of this regulated phosphorylation in the adaptation to ischemia remains to be determined...
Mitochondrial signals initiate the activation of c-Jun N-terminal kinase (JNK) by hypoxia-reoxygenationChristopher J Dougherty
Department of Molecular and Cellular Pharmacology, University of Miami School of Medicine, Miami, Florida 33136, USA
FASEB J 18:1060-70. 2004..The signaling pathway is unique for the reoxygenation stimulus and provides a framework for other non-receptor-mediated pathways of MAPK activation...
