Andre Terzic

Summary

Affiliation: Mayo Clinic
Country: USA

Publications

  1. ncbi Nuclear reprogramming strategy modulates differentiation potential of induced pluripotent stem cells
    Almudena Martinez-Fernandez
    Division of Cardiovascular Diseases, Department of Medicine, Marriott Heart Disease Research Program, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA
    J Cardiovasc Transl Res 4:131-7. 2011
  2. ncbi Genomic chart guiding embryonic stem cell cardiopoiesis
    Randolph S Faustino
    Marriott Heart Disease Research Program, Division of Cardiovascular Diseases, Departments of Medicine, Molecular Pharmacology and Experimental Therapeutics, and Medical Genetics, Mayo Clinic, Rochester, Minnesota 55905, USA
    Genome Biol 9:R6. 2008
  3. ncbi Directed inhibition of nuclear import in cellular hypertrophy
    C Perez-Terzic
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Mayo Foundation, Rochester, Minnesota 55905, USA
    J Biol Chem 276:20566-71. 2001
  4. ncbi Channelopathies: decoding disease pathogenesis
    Andre Terzic
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, MN 55905, USA
    Sci Transl Med 2:42ps37. 2010
  5. ncbi Adenylate Kinase and AMP Signaling Networks: Metabolic Monitoring, Signal Communication and Body Energy Sensing
    Petras Dzeja
    Division of Cardiovascular Disease, Department of Medicine, Mayo Clinic, Rochester, MN 55905, USA E Mail A T
    Int J Mol Sci 10:1729-72. 2009
  6. ncbi Structural plasticity of the cardiac nuclear pore complex in response to regulators of nuclear import
    C Perez-Terzic
    Division of Cardiovascular Diseases and Department of Internal Medicine, Department of Physical Medicine and Rehabilitation, Pharmacology, Mayo Clinic, Rochester, MN, USA
    Circ Res 84:1292-301. 1999
  7. ncbi Embryonic stem cell therapy of heart failure in genetic cardiomyopathy
    Satsuki Yamada
    Department of Medicine, Division of Cardiovascular Diseases, Marriott Heart Disease Research Program, Mayo Clinic, Rochester, Minnesota, USA 55905, USA
    Stem Cells 26:2644-53. 2008
  8. ncbi Reversal of the ATP-liganded state of ATP-sensitive K+ channels by adenylate kinase activity
    J R Elvir-Mairena
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Mayo Foundation, Rochester, Minnesota 55905, USA
    J Biol Chem 271:31903-8. 1996
  9. ncbi Protection conferred by myocardial ATP-sensitive K+ channels in pressure overload-induced congestive heart failure revealed in KCNJ11 Kir6.2-null mutant
    Satsuki Yamada
    Division of Cardiovascular Diseases, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA
    J Physiol 577:1053-65. 2006
  10. ncbi Defective metabolic signaling in adenylate kinase AK1 gene knock-out hearts compromises post-ischemic coronary reflow
    Petras P Dzeja
    Departments of Medicine, Molecular Pharmacology and Experimental Therapeutics, and Medical Genetics, Mayo Clinic, Rochester, Minnesota 55905, USA
    J Biol Chem 282:31366-72. 2007

Research Grants

  1. CARDIOVASOLOGY
    Andre Terzic; Fiscal Year: 2007
  2. Cardiac KATP Channels in Health and Disease
    Andre Terzic; Fiscal Year: 2007
  3. Cardioprotective Repair through Cardiopoiesis
    Andre Terzic; Fiscal Year: 2007
  4. COUPLING OF K ATP CHANNELS WITH CARDIAC ENERGETICS
    Andre Terzic; Fiscal Year: 2003
  5. Cardioprotective Repair through Cardiopoiesis
    Andre Terzic; Fiscal Year: 2010

Detail Information

Publications122 found, 100 shown here

  1. ncbi Nuclear reprogramming strategy modulates differentiation potential of induced pluripotent stem cells
    Almudena Martinez-Fernandez
    Division of Cardiovascular Diseases, Department of Medicine, Marriott Heart Disease Research Program, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA
    J Cardiovasc Transl Res 4:131-7. 2011
    ..Here, we describe the salient components of the reprogramming process and their effect on the downstream differentiation capacity of the iPS populations in the context of cardiovascular regenerative applications...
  2. ncbi Genomic chart guiding embryonic stem cell cardiopoiesis
    Randolph S Faustino
    Marriott Heart Disease Research Program, Division of Cardiovascular Diseases, Departments of Medicine, Molecular Pharmacology and Experimental Therapeutics, and Medical Genetics, Mayo Clinic, Rochester, Minnesota 55905, USA
    Genome Biol 9:R6. 2008
    ..To map molecular patterns critical to cardiogenesis, we interrogated gene expression in stem cells undergoing guided differentiation, and defined a genomic paradigm responsible for confinement of pluripotency...
  3. ncbi Directed inhibition of nuclear import in cellular hypertrophy
    C Perez-Terzic
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Mayo Foundation, Rochester, Minnesota 55905, USA
    J Biol Chem 276:20566-71. 2001
    ..Thus, to overcome the limited capacity for nucleocytoplasmic transport, cells requiring increased nuclear export regulate the nuclear transport pathway by undergoing a metabolic and structural restriction of nuclear import...
  4. ncbi Channelopathies: decoding disease pathogenesis
    Andre Terzic
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, MN 55905, USA
    Sci Transl Med 2:42ps37. 2010
    ..Advances in the molecular medicine of K(ATP) channelopathies offer new perspectives for personalized diagnosis and therapy...
  5. ncbi Adenylate Kinase and AMP Signaling Networks: Metabolic Monitoring, Signal Communication and Body Energy Sensing
    Petras Dzeja
    Division of Cardiovascular Disease, Department of Medicine, Mayo Clinic, Rochester, MN 55905, USA E Mail A T
    Int J Mol Sci 10:1729-72. 2009
    ..Thus, by monitoring energy state and generating and distributing AMP metabolic signals adenylate kinase represents a unique hub within the cellular homeostatic network...
  6. ncbi Structural plasticity of the cardiac nuclear pore complex in response to regulators of nuclear import
    C Perez-Terzic
    Division of Cardiovascular Diseases and Department of Internal Medicine, Department of Physical Medicine and Rehabilitation, Pharmacology, Mayo Clinic, Rochester, MN, USA
    Circ Res 84:1292-301. 1999
    ....
  7. ncbi Embryonic stem cell therapy of heart failure in genetic cardiomyopathy
    Satsuki Yamada
    Department of Medicine, Division of Cardiovascular Diseases, Marriott Heart Disease Research Program, Mayo Clinic, Rochester, Minnesota, USA 55905, USA
    Stem Cells 26:2644-53. 2008
    ..Disclosure of potential conflicts of interest is found at the end of this article...
  8. ncbi Reversal of the ATP-liganded state of ATP-sensitive K+ channels by adenylate kinase activity
    J R Elvir-Mairena
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Mayo Foundation, Rochester, Minnesota 55905, USA
    J Biol Chem 271:31903-8. 1996
    ....
  9. ncbi Protection conferred by myocardial ATP-sensitive K+ channels in pressure overload-induced congestive heart failure revealed in KCNJ11 Kir6.2-null mutant
    Satsuki Yamada
    Division of Cardiovascular Diseases, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA
    J Physiol 577:1053-65. 2006
    ..Thus, K(ATP) channels appear mandatory in acute and chronic cardiac adaptation to imposed haemodynamic load, protecting against congestive heart failure and death...
  10. ncbi Defective metabolic signaling in adenylate kinase AK1 gene knock-out hearts compromises post-ischemic coronary reflow
    Petras P Dzeja
    Departments of Medicine, Molecular Pharmacology and Experimental Therapeutics, and Medical Genetics, Mayo Clinic, Rochester, Minnesota 55905, USA
    J Biol Chem 282:31366-72. 2007
    ..AK1 phosphotransfer thus transduces stress signals into adequate vascular response, providing linkage between cell bioenergetics and coronary flow...
  11. ncbi iPS programmed without c-MYC yield proficient cardiogenesis for functional heart chimerism
    Almudena Martinez-Fernandez
    Marriott Heart Disease Research Program, Division of Cardiovascular Diseases, Departments of Medicine, Molecular Pharmacology and Experimental Therapeutics, and Medical Genetics, Mayo Clinic, Rochester, Minn 55905, USA
    Circ Res 105:648-56. 2009
    ..Induced pluripotent stem cells (iPS) allow derivation of pluripotent progenitors from somatic sources. Originally, iPS were induced by a stemness-related gene set that included the c-MYC oncogene...
  12. ncbi KATP channel knockout worsens myocardial calcium stress load in vivo and impairs recovery in stunned heart
    Richard J Gumina
    Marriott Heart Disease Research Program, Division of Cardiovascular Diseases, Departments of Medicine, Mayo Clinic, Rochester, Minnesota 55905, USA
    Am J Physiol Heart Circ Physiol 292:H1706-13. 2007
    ..Thus K(ATP) channel deficit confers a greater susceptibility to calcium overload in vivo, accentuated in female hearts, impairing contractile recovery under various conditions of high metabolic demand...
  13. ncbi KCNJ11 gene knockout of the Kir6.2 KATP channel causes maladaptive remodeling and heart failure in hypertension
    Garvan C Kane
    Marriott Heart Disease Research Program, Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, MN 55905, USA
    Hum Mol Genet 15:2285-97. 2006
    ..The intact KCNJ11-encoded K(ATP) channel is thus a required safety element preventing hypertension-induced heart failure, with channel dysfunction a molecular substrate for stress-associated channelopathy in cardiovascular disease...
  14. ncbi Cardiac KATP channels in health and disease
    Garvan C Kane
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic College of Medicine, Rochester, MN 55905, USA
    J Mol Cell Cardiol 38:937-43. 2005
    ....
  15. ncbi ATP-sensitive K+ channel channel/enzyme multimer: metabolic gating in the heart
    Alexey E Alekseev
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic College of Medicine, Rochester, MN 55905, USA
    J Mol Cell Cardiol 38:895-905. 2005
    ....
  16. ncbi Cardiopoietic programming of embryonic stem cells for tumor-free heart repair
    Atta Behfar
    Marriott Heart Disease Research Program, Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, MN 55905, USA
    J Exp Med 204:405-20. 2007
    ..Thus, cardiopoietic programming establishes a strategy to hone stem cell pluripotency, offering a tumor-resistant approach for regeneration...
  17. ncbi Knockout of Kir6.2 negates ischemic preconditioning-induced protection of myocardial energetics
    Richard J Gumina
    Department of Internal Medicine, Division of Cardiovascular Diseases, Mayo Clinic, Mayo Foundation, Rochester, Minnesota 55905, USA
    Am J Physiol Heart Circ Physiol 284:H2106-13. 2003
    ..Thus intact K(ATP) channels are integral in ischemic preconditioning-induced protection of cellular energetic dynamics and associated cardiac performance...
  18. ncbi Cellular remodeling in heart failure disrupts K(ATP) channel-dependent stress tolerance
    Denice M Hodgson
    Department of Medicine, Mayo Clinic, Mayo Foundation, Rochester, MN 55905, USA
    EMBO J 22:1732-42. 2003
    ..Thus, disease-induced K(ATP) channel metabolic dysregulation is a contributor to the pathobiology of heart failure, illustrating a mechanism for acquired channelopathy...
  19. ncbi Opposing roles for p16Ink4a and p19Arf in senescence and ageing caused by BubR1 insufficiency
    Darren J Baker
    Department of Pediatric and Adolescent Medicine, Mayo Clinic College of Medicine, Rochester, MN 55905, USA
    Nat Cell Biol 10:825-36. 2008
    ..Thus, we identify BubR1 insufficiency as a trigger for activation of the Cdkn2a locus in certain mouse tissues, and demonstrate that p16(Ink4a) is an effector and p19(Arf) an attenuator of senescence and ageing in these tissues...
  20. ncbi Somatic oxidative bioenergetics transitions into pluripotency-dependent glycolysis to facilitate nuclear reprogramming
    Clifford D L Folmes
    Center for Regenerative Medicine and Marriott Heart Disease Research Program, Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, MN 55905, USA
    Cell Metab 14:264-71. 2011
    ..Thus, the energetic infrastructure of somatic cells transitions into a required glycolytic metabotype to fuel induction of pluripotency...
  21. ncbi Targeting nucleotide-requiring enzymes: implications for diazoxide-induced cardioprotection
    Petras P Dzeja
    Department of Medicine, Mayo Clinic, Mayo Foundation, Rochester, MN 55905, USA
    Am J Physiol Heart Circ Physiol 284:H1048-56. 2003
    ....
  22. ncbi Stable benefit of embryonic stem cell therapy in myocardial infarction
    Denice M Hodgson
    Department of Medicine, Mayo Clinic College of Medicine, Rochester, MN 55905, USA
    Am J Physiol Heart Circ Physiol 287:H471-9. 2004
    ..These findings indicate that embryonic stem cells, through differentiation within the host myocardium, can contribute to a stable beneficial outcome on contractile function and ventricular remodeling in the infarcted heart...
  23. ncbi Administration of allogenic stem cells dosed to secure cardiogenesis and sustained infarct repair
    Atta Behfar
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic College of Medicine, Rochester, MN 55905, USA
    Ann N Y Acad Sci 1049:189-98. 2005
    ..Supported by the host environment, proper dosing and administration of embryonic stem cells is thus here shown useful in the chronic management of cardiac injury promoting sustained repair...
  24. ncbi Genetic disruption of Kir6.2, the pore-forming subunit of ATP-sensitive K+ channel, predisposes to catecholamine-induced ventricular dysrhythmia
    Xiao Ke Liu
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, MN 55905, USA
    Diabetes 53:S165-8. 2004
    ..Thus, intact KATP channel function is mandatory for adequate repolarization under sympathetic stress providing electrical tolerance against triggered arrhythmia...
  25. ncbi ATP-sensitive K+ channel knockout compromises the metabolic benefit of exercise training, resulting in cardiac deficits
    Garvan C Kane
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic College of Medicine, Rochester, MN 55905, USA
    Diabetes 53:S169-75. 2004
    ..Thus, Kir6.2-containing K(ATP) channel activity is required for attainment of the physiologic benefits of exercise training without injury...
  26. ncbi Gene knockout of the KCNJ8-encoded Kir6.1 K(ATP) channel imparts fatal susceptibility to endotoxemia
    Garvan C Kane
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic College of Medicine, Rochester, MN 55905, USA
    FASEB J 20:2271-80. 2006
    ..Thus, the Kir6.1-containing K(ATP) channel, by coupling vasoreactivity with metabolic demand, provides a vital feedback element for cardiovascular tolerance in endotoxic shock...
  27. ncbi Induced pluripotent reprogramming from promiscuous human stemness related factors
    Timothy J Nelson
    Marriott Heart Disease Research Program, Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, MN, USA
    Clin Transl Sci 2:118-26. 2009
    ..Thus, ectopic xeno-transduction across species unmasks the promiscuous nature of stemness induction, suggesting evolutionary selection of core processes for somatic tissue reprogramming...
  28. ncbi Guided cardiopoiesis enhances therapeutic benefit of bone marrow human mesenchymal stem cells in chronic myocardial infarction
    Atta Behfar
    Department of Medicine, Division of Cardiovascular Diseases, Marriott Heart Disease Research Program, Mayo Clinic, Rochester, Minnesota 55905, USA
    J Am Coll Cardiol 56:721-34. 2010
    ..The goal of this study was to guide bone marrow-derived human mesenchymal stem cells (hMSCs) into a cardiac progenitor phenotype and assess therapeutic benefit in chronic myocardial infarction...
  29. ncbi Dynamic phosphometabolomic profiling of human tissues and transgenic models by 18O-assisted ³¹P NMR and mass spectrometry
    Emirhan Nemutlu
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, Minnesota, USA
    Physiol Genomics 44:386-402. 2012
    ..Thus, (18)O-assisted gas chromatography-mass spectrometry and (31)P NMR provide a suitable platform for dynamic phosphometabolomic profiling of the cellular energetic system enabling prediction and diagnosis of metabolic diseases states...
  30. ncbi Decoded calreticulin-deficient embryonic stem cell transcriptome resolves latent cardiophenotype
    Randolph S Faustino
    Marriott Heart Disease Research Program, Division of Cardiovascular Diseases, Departments of Medicine, Molecular Pharmacology and Experimental Therapeutics, and Medical Genetics, Mayo Clinic, Rochester, Minnesota 55905, USA
    Stem Cells 28:1281-91. 2010
    ....
  31. ncbi Proteomic profiling of KATP channel-deficient hypertensive heart maps risk for maladaptive cardiomyopathic outcome
    Jelena Zlatkovic
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, MN 55905, USA
    Proteomics 9:1314-25. 2009
    ..Thus, Kir6.2 ablation engenders unfavorable proteomic remodeling in hypertensive hearts, providing a composite molecular substrate for pathologic stress-associated cardiovascular disease...
  32. ncbi Kir6.2 is required for adaptation to stress
    Leonid V Zingman
    Division of Cardiovascular Diseases, Departments of Medicine and Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN 55905, USA
    Proc Natl Acad Sci U S A 99:13278-83. 2002
    ..In the absence of Kir6.2, vigorous sympathetic challenge caused arrhythmia and sudden death, preventable by calcium-channel blockade. Thus, this vital function identifies a physiological role for K(ATP) channels in the heart...
  33. ncbi Role for SUR2A ED domain in allosteric coupling within the K(ATP) channel complex
    Amy B Karger
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, MN 55905, USA
    J Gen Physiol 131:185-96. 2008
    ....
  34. ncbi Mapping hypoxia-induced bioenergetic rearrangements and metabolic signaling by 18O-assisted 31P NMR and 1H NMR spectroscopy
    Darko Pucar
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Mayo Foundation, Rochester, MN 55905, USA
    Mol Cell Biochem 256:281-9. 2004
    ..Thus, 18O-assisted 31P NMR combined with 1H NMR provide a powerful approach in capturing rearrangements in cardiac bioenergetics, and associated metabolic signaling that underlie the cardiac adaptive response to stress...
  35. ncbi SDF-1-enhanced cardiogenesis requires CXCR4 induction in pluripotent stem cells
    Anca Chiriac
    Marriott Heart Disease Research Program, Division of Cardiovascular Diseases, Department of Medical Genetics, Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA
    J Cardiovasc Transl Res 3:674-82. 2010
    ..Thus, a pro-cardiogenic signaling role for the CXCR4/SDF1 axis is herein revealed within pluripotent stem cell progenitors, exposing a functional target to promote lineage-specific differentiation...
  36. ncbi Targeted disruption of K(ATP) channels aggravates cardiac toxicity in cocaine abuse
    Santiago Reyes
    Department of Medicine, Mayo Clinic, Rochester, Minnesota, USA
    Clin Transl Sci 2:361-5. 2009
    ..This study therefore reveals a previously unrecognized role of Kir6.2-encoded K(ATP) channels in determining cardiovascular outcome in chronic cocaine abuse, identifying a novel molecular determinant of cocaine cardiotoxicity...
  37. ncbi Kv1.5 channelopathy due to KCNA5 loss-of-function mutation causes human atrial fibrillation
    Timothy M Olson
    Department of Medicine, Division of Cardiovascular Diseases, Mayo Clinic College of Medicine, Rochester, MN 55905, USA
    Hum Mol Genet 15:2185-91. 2006
    ..This first report of Kv1.5 loss-of-function channelopathy establishes KCNA5 mutation as a novel risk factor for repolarization deficiency and atrial fibrillation...
  38. ncbi Coupling of cell energetics with membrane metabolic sensing. Integrative signaling through creatine kinase phosphotransfer disrupted by M-CK gene knock-out
    M Roselle Abraham
    Division of Cardiovascular Diseases, Departments of Medicine, Molecular Pharmacology, and Experimental Therapeutics, Mayo Clinic, Rochester, Minnesota 55905, USA
    J Biol Chem 277:24427-34. 2002
    ..Thus, in the compartmentalized cell environment, phosphotransfer systems shunt diffusional barriers and secure regimented signal transduction integrating metabolic sensors with the cellular energetic network...
  39. ncbi Progenitor cell therapy in a porcine acute myocardial infarction model induces cardiac hypertrophy, mediated by paracrine secretion of cardiotrophic factors including TGFbeta1
    Brendan Doyle
    Division of Cardiovascular Diseases, Mayo Clinic College of Medicine, Rochester, Minnesota, USA
    Stem Cells Dev 17:941-51. 2008
    ....
  40. ncbi Electron spray ionization mass spectrometry and 2D 31P NMR for monitoring 18O/16O isotope exchange and turnover rates of metabolic oligophosphates
    Emirhan Nemutlu
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, MN 55905, USA
    Anal Bioanal Chem 403:697-706. 2012
    ..Such method is advantageous for large scale dynamic phosphometabolomic profiling of metabolic networks and acquiring information on the status of probed cellular energetic system...
  41. ncbi KATP channel mutation confers risk for vein of Marshall adrenergic atrial fibrillation
    Timothy M Olson
    Marriott Heart Disease Research Program, Division of Cardiovascular Diseases, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA
    Nat Clin Pract Cardiovasc Med 4:110-6. 2007
    ..In the absence of traditional risk factors for disease, a genetic defect in electrical homeostasis underlying stress-induced AF was explored...
  42. ncbi Aging and cardioprotection
    Arshad Jahangir
    Marriott Heart Disease Research Program, Division of Cardiovascular Diseases, and Department of Medicine, Mayo Clinic College of Medicine, Rochester, MN 55905, USA
    J Appl Physiol 103:2120-8. 2007
    ....
  43. ncbi Lineage specification of Flk-1+ progenitors is associated with divergent Sox7 expression in cardiopoiesis
    Timothy J Nelson
    Marriott Heart Disease Research Program, Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA
    Differentiation 77:248-55. 2009
    ..Thus, differential Sox7 gene expression presents a novel biomarker profile, and possible regulatory switch, to distinguish cardiovascular pedigrees within Flk-1(+) multi-lineage progenitors...
  44. ncbi c-MYC independent nuclear reprogramming favors cardiogenic potential of induced pluripotent stem cells
    Almudena Martinez-Fernandez
    Division of Cardiovascular Diseases, Departments of Medicine, Mayo Clinic, Rochester, MN, USA
    J Cardiovasc Transl Res 3:13-23. 2010
    ..Thus, nuclear reprogramming independent of c-MYC enhances production of pluripotent stem cells with innate cardiogenic potential...
  45. ncbi Increased expression of BubR1 protects against aneuploidy and cancer and extends healthy lifespan
    Darren J Baker
    Department of Pediatric and Adolescent Medicine, Mayo Clinic, 200 First Street Southwest, Rochester, Minnesota 55905, USA
    Nat Cell Biol 15:96-102. 2013
    ..Collectively, these data uncover a generalized function for BubR1 in counteracting defects that cause whole-chromosome instability and suggest that modulating BubR1 provides a unique opportunity to extend healthy lifespan...
  46. ncbi Developmental enhancement of adenylate kinase-AMPK metabolic signaling axis supports stem cell cardiac differentiation
    Petras P Dzeja
    Marriott Heart Disease Research Program, Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, Minnesota, United States of America
    PLoS ONE 6:e19300. 2011
    ..Adenylate kinase (AK) and associated AMP-activated protein kinase (AMPK) constitute a major metabolic signaling axis, yet the role of this system in guiding differentiation and lineage specification remains undefined...
  47. ncbi Bioenergetic protection of failing atrial and ventricular myocardium by vasopeptidase inhibitor omapatrilat
    Yong-Mei Cha
    Department of Medicine, Mayo Clinic, Rochester, MN 55905, USA
    Am J Physiol Heart Circ Physiol 290:H1686-92. 2006
    ..Thus therapy with omapatrilat demonstrates the benefit in protecting phosphotransfer enzyme activities and in preventing impairment of atrial and ventricular bioenergetics in heart failure...
  48. ncbi Cardiogenic induction of pluripotent stem cells streamlined through a conserved SDF-1/VEGF/BMP2 integrated network
    Anca Chiriac
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, Minnesota, United States of America
    PLoS ONE 5:e9943. 2010
    ..As embryonic stem cells respond concomitantly to diverse signaling pathways during differentiation, extraction of a pro-cardiogenic network would offer a roadmap to streamline cardiac progenitor output...
  49. ncbi Transgenic overexpression of human DMPK accumulates into hypertrophic cardiomyopathy, myotonic myopathy and hypotension traits of myotonic dystrophy
    D Fearghas O'Cochlain
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic College of Medicine, Rochester, MN 55905, USA
    Hum Mol Genet 13:2505-18. 2004
    ..Proper expression of hDMPK is, therefore, mandatory in supporting the integral balance among cytoarchitectural infrastructure, ion-homeostasis and viability control in various muscle cell types...
  50. ncbi Aging-induced alterations in gene transcripts and functional activity of mitochondrial oxidative phosphorylation complexes in the heart
    Claudia C Preston
    Marriot Heart Disease Research Program, Department of Medicine, Mayo Clinic, Rochester, MN 55905, United States
    Mech Ageing Dev 129:304-12. 2008
    ....
  51. ncbi Mitochondrial tolerance to stress impaired in failing heart
    Cevher Ozcan
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic and Foundation, Guggenheim 7F, Rochester, MN 55905, USA
    J Mol Cell Cardiol 35:1161-6. 2003
    ..This abnormal vulnerability to stress underscores the impact of mitochondrial dysfunction in the pathobiology of heart failure...
  52. ncbi Failing atrial myocardium: energetic deficits accompany structural remodeling and electrical instability
    Yong-Mei Cha
    Division of Cardiovascular Diseases, Department of Internal Medicine, Mayo Clinic and Foundation, Rochester, Minnesota 55905, USA
    Am J Physiol Heart Circ Physiol 284:H1313-20. 2003
    ..Myocardial bioenergetic deficits are a conserved feature of dysfunctional atrial and ventricular myocardium in CHF and may constitute a component of the substrate for AF in CHF...
  53. ncbi Adenylate kinase AK1 knockout heart: energetics and functional performance under ischemia-reperfusion
    Darko Pucar
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic and Foundation, Rochester, MN 55905, USA
    Am J Physiol Heart Circ Physiol 283:H776-82. 2002
    ..Thus deletion of the AK1 gene reveals that adenylate kinase phosphotransfer supports myocardial function on initiation of ischemic stress and safeguards intracellular nucleotide pools in postischemic recovery...
  54. ncbi ABCC9 mutations identified in human dilated cardiomyopathy disrupt catalytic KATP channel gating
    Martin Bienengraeber
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic College of Medicine, Mayo Foundation, Rochester, Minnesota 55905, USA
    Nat Genet 36:382-7. 2004
    ..Defective catalysis-mediated pore regulation is thus a mechanism for channel dysfunction and susceptibility to dilated cardiomyopathy...
  55. ncbi Interaction of asymmetric ABCC9-encoded nucleotide binding domains determines KATP channel SUR2A catalytic activity
    Sungjo Park
    Marriott Heart Disease Research Program, Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, Minnesota 55905, USA
    J Proteome Res 7:1721-8. 2008
    ....
  56. ncbi Stem cells transform into a cardiac phenotype with remodeling of the nuclear transport machinery
    Carmen Perez Terzic
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic College of Medicine, Rochester, MN 55905, USA
    Nat Clin Pract Cardiovasc Med 4:S68-76. 2007
    ....
  57. ncbi Nucleotide-gated KATP channels integrated with creatine and adenylate kinases: amplification, tuning and sensing of energetic signals in the compartmentalized cellular environment
    Vitaliy A Selivanov
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Guggenheim, Rochester, MN 55905, USA
    Mol Cell Biochem 256:243-56. 2004
    ....
  58. ncbi Guided stem cell cardiopoiesis: discovery and translation
    Atta Behfar
    Marriott Heart Disease Research Program, Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, MN 55905, USA
    J Mol Cell Cardiol 45:523-9. 2008
    ..With appropriate validation of this newly derived cardiopoietic phenotype, the next generation of trials should achieve demonstrable benefit across patient populations...
  59. ncbi Sarcolemmal ATP-sensitive K(+) channels control energy expenditure determining body weight
    Alexey E Alekseev
    Department of Medicine, Mayo Clinic, Rochester, MN 55905, USA
    Cell Metab 11:58-69. 2010
    ....
  60. ncbi Platelet lysate consisting of a natural repair proteome supports human mesenchymal stem cell proliferation and chromosomal stability
    Ruben Crespo-Diaz
    Division of Cardiovascular Diseases, Departments of Medicine and Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN, USA
    Cell Transplant 20:797-811. 2011
    ..Thus, GMP-adherent human platelet lysate accelerates hMSC proliferation with no chromosomal aberrancy, through an innate repair paradigm...
  61. ncbi Induced pluripotent stem cells: developmental biology to regenerative medicine
    Timothy J Nelson
    Marriott Heart Disease Research Program, Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA
    Nat Rev Cardiol 7:700-10. 2010
    ..Thus, the principles of cardiogenesis can now be applied to regenerative medicine in order to optimize personalized therapeutics, diagnostics, and discovery-based science for the development of novel clinical applications...
  62. ncbi Repair of acute myocardial infarction by human stemness factors induced pluripotent stem cells
    Timothy J Nelson
    Mayo Clinic, 200 First St SW, Rochester, MN 55905, USA
    Circulation 120:408-16. 2009
    ..Induced pluripotent stem cells (iPS) demonstrate aptitude for de novo cardiac differentiation, yet their potential for heart disease therapy has not been tested...
  63. ncbi Human K(ATP) channelopathies: diseases of metabolic homeostasis
    Timothy M Olson
    Marriott Heart Disease Research Program, Division of Cardiovascular Diseases, Department of Internal Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA
    Pflugers Arch 460:295-306. 2010
    ..Thus, advances in molecular medicine in the emerging field of human KATP channelopathies offer new opportunities for targeted individualized screening, early diagnosis, and tailored therapy...
  64. ncbi K(ATP) channel polymorphism is associated with left ventricular size in hypertensive individuals: a large-scale community-based study
    Santiago Reyes
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, MN, USA
    Hum Genet 123:665-7. 2008
    ..These findings implicate Kir6.2 K23 as a risk factor for adverse subclinical myocardial remodeling, and underscore the significance of cardiac K(ATP) channels within the population...
  65. ncbi Energetic communication between mitochondria and nucleus directed by catalyzed phosphotransfer
    Petras P Dzeja
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, MN 55905, USA
    Proc Natl Acad Sci U S A 99:10156-61. 2002
    ..Thus, mitochondrial oxidative phosphorylation coupled with phosphotransfer relays provides an efficient energetic unit in support of nuclear transport...
  66. ncbi Mitochondrial oxidative metabolism is required for the cardiac differentiation of stem cells
    Susan Chung
    Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN 55905, USA
    Nat Clin Pract Cardiovasc Med 4:S60-7. 2007
    ..Mitochondria-dependent energetic circuits are thus critical regulators of de novo cardiogenesis and targets for heart regeneration...
  67. ncbi Developmental restructuring of the creatine kinase system integrates mitochondrial energetics with stem cell cardiogenesis
    Susan Chung
    Marriott Heart Disease Research Program, Division of Cardiovascular Diseases, Department of Medicine, Molecular Pharmacology and Experimental Therapeutics and Medical Genetics, Mayo Clinic, Rochester, MN 55905, USA
    Ann N Y Acad Sci 1147:254-63. 2008
    ..Thus, the evolving CK-catalyzed phosphotransfer network integrates mitochondrial energetics with cardiogenic programming, securing the emergence of energy-consuming cardiac functions in differentiating embryonic stem cells...
  68. ncbi Tandem function of nucleotide binding domains confers competence to sulfonylurea receptor in gating ATP-sensitive K+ channels
    Leonid V Zingman
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Mayo Foundation, Rochester, Minnesota 55905, USA
    J Biol Chem 277:14206-10. 2002
    ..These findings provide a paradigm of K(ATP) channel gating based on integration of both NBDs into a functional unit within the multimeric channel complex...
  69. ncbi Potassium channel openers protect cardiac mitochondria by attenuating oxidant stress at reoxygenation
    Cevher Ozcan
    Department of Medicine, Molecular Pharmacology, and Experimental Therapeutics, Mayo Clinic, Mayo Foundation, Rochester, Minnesota 55905, USA
    Am J Physiol Heart Circ Physiol 282:H531-9. 2002
    ..Thus the cardioprotecive mechanism of K(+) channel openers includes direct attenuation of mitochondrial oxidant stress at reoxygenation...
  70. ncbi Adenylate kinase phosphotransfer communicates cellular energetic signals to ATP-sensitive potassium channels
    A J Carrasco
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Mayo Foundation, Guggenheim 7, 200 First Street Southwest, Rochester, MN 55905, USA
    Proc Natl Acad Sci U S A 98:7623-8. 2001
    ..Assigning a signal processing role to adenylate kinase identifies a phosphorelay mechanism essential for efficient coupling of cellular energetics with K(ATP) channels and associated functions...
  71. ncbi Signaling in channel/enzyme multimers: ATPase transitions in SUR module gate ATP-sensitive K+ conductance
    L V Zingman
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Mayo Foundation Rochester, MN 55905, USA
    Neuron 31:233-45. 2001
    ..Signal transduction through the catalytic module provides a paradigm for channel/enzyme operation and integrates membrane excitability with metabolic cascades...
  72. ncbi Cardiac cell repair therapy: a clinical perspective
    Bernard J Gersh
    Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN 55905, USA
    Mayo Clin Proc 84:876-92. 2009
    ..An interdisciplinary effort across the scientific and clinical community within academia, biotechnology, and government will drive the successful realization of this next generation of therapeutic agents for the "broken" heart...
  73. ncbi Both systolic and diastolic dysfunction characterize nonischemic inhibition of myocardial energy metabolism: an experimental strain rate echocardiographic study
    Josef Korinek
    Department of Internal Medicine, Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN 55905, USA
    J Am Soc Echocardiogr 17:1239-44. 2004
    ..CONCLUSIONS: Regional inhibition of myocyte energetics leads to both systolic and diastolic dysfunction by SR echocardiography, but the presence of a residual phosphotransfer protects microstructural integrity...
  74. ncbi (31)P NMR correlation maps of (18)O/ (16)O chemical shift isotopic effects for phosphometabolite labeling studies
    Nenad Juranic
    Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN, 55905, USA
    J Biomol NMR 50:237-45. 2011
    ..The biological usefulness of the J-decoupled (31)P NMR 2D chemical shift correlation maps was validated on adenosine tri-phosphate fractionally (18)O labeled in perfused mammalian hearts...
  75. ncbi Spontaneous myocarditis mimicking human disease occurs in the presence of an appropriate MHC and non-MHC background in transgenic mice
    Veena Taneja
    Department of Immunology, Mayo Clinic College of Medicine, 200 First Street S W, Rochester, MN 55905, USA
    J Mol Cell Cardiol 42:1054-64. 2007
    ..This model of myocarditis occurs predominantly in female mice and may provide insight into the pathogenesis of heart disease in women...
  76. ncbi Cardioprotective repair through stem cell-based cardiopoiesis
    Atta Behfar
    Marriott Heart Disease Research Program, Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, Minnesota 55905, USA
    J Appl Physiol 103:1438-40. 2007
    ..Here, we examine the recent application of genomic and proteomic technology to decipher the process of cardiopoiesis and to recruit cardiopoietic stem cells for cardioprotection and safe myocardial repair...
  77. ncbi Age- and sex-related atrial electrophysiologic and structural changes
    Xiao-Ke Liu
    Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic, Rochester, Minnesota 55905, USA
    Am J Cardiol 94:373-5. 2004
    ..It was concluded that LA size is greater in the elderly and in men, which may increase their risk for AF...
  78. ncbi Phosphotransfer networks and cellular energetics
    Petras P Dzeja
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Mayo Foundation, Rochester, MN 55905, USA
    J Exp Biol 206:2039-47. 2003
    ....
  79. ncbi Phosphotransfer dynamics in skeletal muscle from creatine kinase gene-deleted mice
    Petras P Dzeja
    Department of Biochemistry, University of Minnesota, Minneapolis, MN, USA
    Mol Cell Biochem 256:13-27. 2004
    ..Thus, redistribution of phosphotransfer through glycolytic and AK networks contributes to energetic homeostasis in muscles under genetic and metabolic stress complementing loss of CK function...
  80. ncbi K(ATP) channel therapeutics at the bedside
    A Jahangir
    Division of Cardiovascular Diseases, Departmentof Medicine, Mayo Clinic College of Medicine, Guggenheim 7, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA
    J Mol Cell Cardiol 39:99-112. 2005
    ....
  81. ncbi Network systems biology for drug discovery
    D K Arrell
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, Minnesota, USA
    Clin Pharmacol Ther 88:120-5. 2010
    ....
  82. ncbi Potassium channel openers: therapeutic potential in cardiology and medicine
    A Jahangir
    Division of Cardiovascular Disease, Department of Medicine, Mayo Clinic, Rochester, MN 55905, USA
    Expert Opin Pharmacother 2:1995-2010. 2001
    ..However, clinical experience with these drugs is limited and their place in patient management needs to be fully established...
  83. ncbi Mechanical unloading versus neurohumoral stimulation on myocardial structure and endocrine function In vivo
    O Lisy
    Division of Cardiovascular Diseases, Departments of Internal Medicine and Physiology, Mayo Clinic and Foundation, Rochester, MN, USA
    Circulation 102:338-43. 2000
    ..CONCLUSIONS-Chronic mechanical unloading of the heart results in myocardial atrophy and lack of activation of ANP synthesis despite marked neurohumoral stimulation by the growth promoters ET and Ang II...
  84. ncbi The modulating actions of sulfonylurea on atrial natriuretic peptide release in experimental acute heart failure
    H H Chen
    Cardiorenal and Cardiovascular Research Laboratories, Division of Cardiovascular Diseases, Departments of Medicine, Physiology and Pharmacology, Mayo Clinic, Mayo Foundation, Rochester, MN 55905, USA
    Eur J Heart Fail 2:33-40. 2000
    ..This study defined the modulating actions of sulfonylurea on acute release of atrial natriuretic peptide (ANP) in experimental acute heart failure...
  85. ncbi Aminoglycoside-induced translational read-through in disease: overcoming nonsense mutations by pharmacogenetic therapy
    L V Zingman
    Marriott Heart Disease Research Program, Department of Medicine, Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota, USA
    Clin Pharmacol Ther 81:99-103. 2007
    ..The challenge ahead is to maximize efficacy while preventing interaction with normal protein production and function...
  86. ncbi Bioinformatic networks: molecular reticles for pinpointing pharmacological target selection
    R S Faustino
    Marriott Heart Disease Research Program, Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, Minnesota, USA
    Clin Pharmacol Ther 84:543-5. 2008
    ..Translational implementation holds potential for increased therapeutic specificity and offers opportunities to add value to drug discovery and development through facilitation of individualized treatment...
  87. ncbi Comparative analysis of the kinetic characteristics of L-type calcium channels in cardiac cells of hibernators
    A E Alekseev
    Institute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Pushchino, Russia
    Biophys J 70:786-97. 1996
    ..This suggests that during hibernation additional mechanisms may reduce the single Ca2+ channel-conductance and/or keep a fraction of the cardiac L-type Ca2+ channel population in a non-active state...
  88. ncbi Restoration of Ca2+-inhibited oxidative phosphorylation in cardiac mitochondria by mitochondrial Ca2+ unloading
    E L Holmuhamedov
    Department of Medicine, Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Mayo Foundation, Rochester, MN 55905, USA
    Mol Cell Biochem 220:135-40. 2001
    ..This study, therefore, identifies an effective strategy capable to rescue Ca2+-disrupted mitochondrial energetics...
  89. ncbi Increased calcium vulnerability of senescent cardiac mitochondria: protective role for a mitochondrial potassium channel opener
    A Jahangir
    Division of Cardiovascular Diseases, Departments of Medicine, Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Mayo Foundation, Guggenheim 7, Rochester, MN 55905, USA
    Mech Ageing Dev 122:1073-86. 2001
    ..In this way, the present study identifies the potential usefulness for pharmacotherapy in protecting vulnerable senescent mitochondria from conditions of Ca2+ overload, such as ischemia-reperfusion...
  90. ncbi K(ATP) channel pharmacogenomics: from bench to bedside
    S Sattiraju
    Marriott Heart Disease Research Program, Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, Minnesota, USA
    Clin Pharmacol Ther 83:354-7. 2008
    ..There is an increased recognition that genetic variability of the K(ATP) channel impacts therapeutic decision-making in human disease...
  91. ncbi G proteins activate ATP-sensitive K+ channels by antagonizing ATP-dependent gating
    A Terzic
    Department of Internal Medicine, Mayo Clinic, Rochester, Minnesota 55905
    Neuron 12:885-93. 1994
    ..G proteins stimulate cardiac KATP channels apparently by antagonizing ATPi-dependent inhibitory gating. Regulation of ligand-dependent gating represents a distinct type of G protein modulation of ion channels...
  92. ncbi Diazoxide protects mitochondria from anoxic injury: implications for myopreservation
    C Ozcan
    Division of Cardiovascular Diseases and the Department of Medicine, Mayo Clinic and Foundation, Rochester, MN 55905, USA
    J Thorac Cardiovasc Surg 121:298-306. 2001
    ..By protecting mitochondria and preserving myocardial energetics, diazoxide may be useful under conditions of reduced oxygen availability, including global surgical ischemia or storage of donor heart...
  93. ncbi Doppler strain imaging closely reflects myocardial energetic status in acute progressive ischemia and indicates energetic recovery after reperfusion
    Josef Korinek
    Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota, USA
    J Am Soc Echocardiogr 21:961-8. 2008
    ....
  94. ncbi Derivation of a cardiopoietic population from human mesenchymal stem cells yields cardiac progeny
    Atta Behfar
    Department of Medicine, Mayo Clinic College of Medicine, Rochester, MN 55905, USA
    Nat Clin Pract Cardiovasc Med 3:S78-82. 2006
    ..Maximizing the cardiogenic potential of human mesenchymal stem cells achieves a critical step in optimizing therapeutic translation...
  95. ncbi KCNJ11 knockout morula re-engineered by stem cell diploid aggregation
    Timothy J Nelson
    Departments of Medicine, Marriott Heart Disease Research Program, Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN 55905, USA
    Philos Trans R Soc Lond B Biol Sci 364:269-76. 2009
    ..The development of adult chimerism from the knockout<-->wild-type mosaic embryo offers thereby a new paradigm to probe the ecogenetic control of the KATP channel-dependent stress response...
  96. ncbi Quaternary structure of KATP channel SUR2A nucleotide binding domains resolved by synchrotron radiation X-ray scattering
    Sungjo Park
    Marriott Heart Disease Research Program, Division of Cardiovascular Diseases, Departments of Medicine, Molecular Pharmacology and Experimental Therapeutics, and Medical Genetics, Mayo Clinic, Rochester, MN 55905, USA
    J Struct Biol 169:243-51. 2010
    ..The resolved quaternary structure delineates thereby a macromolecular arrangement of K(ATP) channel SUR2A regulatory domains...
  97. ncbi Human endothelial progenitor cells tolerate oxidative stress due to intrinsically high expression of manganese superoxide dismutase
    Tongrong He
    Department of Anesthesiology, Mayo Clinic, Rochester, Minn 55905, USA
    Arterioscler Thromb Vasc Biol 24:2021-7. 2004
    ..CONCLUSIONS: Human EPCs are resistant to oxidative stress. High intrinsic expression of MnSOD is a critical mechanism protecting EPCs against oxidative stress...
  98. ncbi Compromised energetics in the adenylate kinase AK1 gene knockout heart under metabolic stress
    D Pucar
    Division of Cardiovascular Diseases, Departments of Medicine, Molecular Pharmacology and Experimental Therapeutics, and Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota 55905, USA
    J Biol Chem 275:41424-9. 2000
    ..This study, therefore, provides first direct evidence that AK1 is essential in maintaining myocardial energetic homeostasis, in particular under metabolic stress...
  99. ncbi Cellular energetics in the preconditioned state: protective role for phosphotransfer reactions captured by 18O-assisted 31P NMR
    D Pucar
    Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Mayo Foundation, Rochester, Minnesota 55905, USA
    J Biol Chem 276:44812-9. 2001
    ..Thus, the plasticity of phosphotransfer networks contributes to the effective functioning of the cellular energetic system, providing a mechanism for increased tolerance toward injury...
  100. ncbi Acquired resistance of a mammalian cell line to hypoxia-reoxygenation through cotransfection of Kir6.2 and SUR1 clones
    A Jovanovic
    Department of Internal Medicine, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55905, USA
    Lab Invest 78:1101-7. 1998
    ..The findings from this study may, thus, provide a framework for future therapeutic strategies based on gene delivery of KATP channel subunits in cells and tissues vulnerable to hypoxia-reoxygenation insults...
  101. ncbi Physical association between recombinant cardiac ATP-sensitive K+ channel subunits Kir6.2 and SUR2A
    E Lorenz
    Department of Internal Medicine, Mayo Clinic, Mayo Foundation, Rochester, Minnesota 55905, USA
    J Mol Cell Cardiol 31:425-34. 1999
    ..The demonstration of complex formation between Kir6.2 and SUR2A indicates that the structural basis for channel function may rely on direct physical interaction of the two subunits...

Research Grants15

  1. CARDIOVASOLOGY
    Andre Terzic; Fiscal Year: 2007
    ....
  2. Cardiac KATP Channels in Health and Disease
    Andre Terzic; Fiscal Year: 2007
    ..Thus, this proposal will provide an integrated understanding of cardiac KATP channels in metabolic signal decoding, stress adaptation, and their impact for clinical medicine. ..
  3. Cardioprotective Repair through Cardiopoiesis
    Andre Terzic; Fiscal Year: 2007
    ..Dissection of cardiogenesis at the molecular and cellular level will be further integrated into a therapeutic paradigm, and translated to the organ and organism level for safe cell-based regenerative therapy of myocardial infarction. ..
  4. COUPLING OF K ATP CHANNELS WITH CARDIAC ENERGETICS
    Andre Terzic; Fiscal Year: 2003
    ..Such concept is of fundamental importance in channel biology, and essential to understand cellular regulation and protection under metabolic stress. ..
  5. Cardioprotective Repair through Cardiopoiesis
    Andre Terzic; Fiscal Year: 2010
    ..abstract_text> ..