M E Anderson

Summary

Affiliation: Vanderbilt University
Country: USA

Publications

  1. ncbi request reprint Calmodulin kinase signaling in heart: an intriguing candidate target for therapy of myocardial dysfunction and arrhythmias
    Mark E Anderson
    Vanderbilt University Medical Center, 383 Preston Research Building, Nashville, TN 37232 6300, USA
    Pharmacol Ther 106:39-55. 2005
  2. ncbi request reprint QT interval prolongation and arrhythmia: an unbreakable connection?
    M E Anderson
    Department of Cardiovascular Medicine, Vanderbilt University Medical School, Nashville, TN, USA
    J Intern Med 259:81-90. 2006
  3. ncbi request reprint Calmodulin kinase and L-type calcium channels; a recipe for arrhythmias?
    Mark E Anderson
    Division of Cardiovascular Medicine, Departments of Medicine and Pharmacology, Vanderbilt University Medical Center, 383 Preston Research Building, 2220 Pierce Avenue, Nashville, TN 37232 6300, USA
    Trends Cardiovasc Med 14:152-61. 2004
  4. pmc Calmodulin kinase is a molecular switch for cardiac excitation-contraction coupling
    Y Wu
    Department of Internal Medicine, Vanderbilt University, Nashville, TN 37232, USA
    Proc Natl Acad Sci U S A 98:2877-81. 2001
  5. ncbi request reprint Calmodulin inhibitor W-7 unmasks a novel electrocardiographic parameter that predicts initiation of torsade de pointes
    T David Gbadebo
    Department of Medicine, Vanderbilt University Medical Center, Nashville, Tenn 37232 6300, USA
    Circulation 105:770-4. 2002
  6. ncbi request reprint Calmodulin kinase II and arrhythmias in a mouse model of cardiac hypertrophy
    Yuejin Wu
    Department of Internal Medicine, Vanderbilt University, Nashville, Tenn, USA
    Circulation 106:1288-93. 2002
  7. ncbi request reprint Calmodulin and the philosopher's stone: Changing Ca2+ into arrhythmias
    Mark E Anderson
    Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee 37232 6300, USA
    J Cardiovasc Electrophysiol 13:195-7. 2002
  8. ncbi request reprint Cardiac ion channels
    Dan M Roden
    Departments of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA
    Annu Rev Physiol 64:431-75. 2002
  9. ncbi request reprint Cardiac repolarization: current knowledge, critical gaps, and new approaches to drug development and patient management
    Mark E Anderson
    Vanderbilt University Medical Center, Nashville, Tenn 37232 6300, USA
    Am Heart J 144:769-81. 2002
  10. ncbi request reprint Frequency of late recurrence of intra-atrial reentry tachycardia after radiofrequency catheter ablation in patients with congenital heart disease
    Prince J Kannankeril
    Department of Medicine, Vanderbilty University Medical Center, Nashville, Tennessee 37232 2572, USA
    Am J Cardiol 92:879-81. 2003

Collaborators

Detail Information

Publications57

  1. ncbi request reprint Calmodulin kinase signaling in heart: an intriguing candidate target for therapy of myocardial dysfunction and arrhythmias
    Mark E Anderson
    Vanderbilt University Medical Center, 383 Preston Research Building, Nashville, TN 37232 6300, USA
    Pharmacol Ther 106:39-55. 2005
    ..This review discusses CaMKII structure and function and recent evidence implicating CaMKII inhibition as a potential strategy for treating myocardial dysfunction and arrhythmias in the setting of structural heart disease...
  2. ncbi request reprint QT interval prolongation and arrhythmia: an unbreakable connection?
    M E Anderson
    Department of Cardiovascular Medicine, Vanderbilt University Medical School, Nashville, TN, USA
    J Intern Med 259:81-90. 2006
    ..CaMKII is one of these molecules and CaMKII activity is at least partially responsible for the proarrhythmic consequences of excessive QT interval prolongation...
  3. ncbi request reprint Calmodulin kinase and L-type calcium channels; a recipe for arrhythmias?
    Mark E Anderson
    Division of Cardiovascular Medicine, Departments of Medicine and Pharmacology, Vanderbilt University Medical Center, 383 Preston Research Building, 2220 Pierce Avenue, Nashville, TN 37232 6300, USA
    Trends Cardiovasc Med 14:152-61. 2004
    ..LTCC dysregulation is discussed in the context of new results showing that CaMKII can be a proarrhythmic signal in disease conditions in which Ca2+(i) is disordered and cardiac repolarization is excessively prolonged...
  4. pmc Calmodulin kinase is a molecular switch for cardiac excitation-contraction coupling
    Y Wu
    Department of Internal Medicine, Vanderbilt University, Nashville, TN 37232, USA
    Proc Natl Acad Sci U S A 98:2877-81. 2001
    ..These findings support the hypothesis that CaMK is required to functionally couple LTCC and RyR during cardiac ECC...
  5. ncbi request reprint Calmodulin inhibitor W-7 unmasks a novel electrocardiographic parameter that predicts initiation of torsade de pointes
    T David Gbadebo
    Department of Medicine, Vanderbilt University Medical Center, Nashville, Tenn 37232 6300, USA
    Circulation 105:770-4. 2002
    ..ECGs were analyzed from a well-characterized animal model of TdP to identify more reliable predictors of this life-threatening ventricular arrhythmia...
  6. ncbi request reprint Calmodulin kinase II and arrhythmias in a mouse model of cardiac hypertrophy
    Yuejin Wu
    Department of Internal Medicine, Vanderbilt University, Nashville, Tenn, USA
    Circulation 106:1288-93. 2002
    ..CaMKII upregulation and prolonged repolarization are general features of cardiomyopathy, but the role of CaMKII in arrhythmias in cardiomyopathy is unknown...
  7. ncbi request reprint Calmodulin and the philosopher's stone: Changing Ca2+ into arrhythmias
    Mark E Anderson
    Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee 37232 6300, USA
    J Cardiovasc Electrophysiol 13:195-7. 2002
    ..This article will examine the implications of these recent findings for arrhythmogenesis and the development of new antiarrhythmic therapies...
  8. ncbi request reprint Cardiac ion channels
    Dan M Roden
    Departments of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA
    Annu Rev Physiol 64:431-75. 2002
    ..This review discusses these new tools and how their application to the problem of arrhythmias is generating new mechanistic insights to identify patients at risk for this condition and developing improved antiarrhythmic therapies...
  9. ncbi request reprint Cardiac repolarization: current knowledge, critical gaps, and new approaches to drug development and patient management
    Mark E Anderson
    Vanderbilt University Medical Center, Nashville, Tenn 37232 6300, USA
    Am Heart J 144:769-81. 2002
  10. ncbi request reprint Frequency of late recurrence of intra-atrial reentry tachycardia after radiofrequency catheter ablation in patients with congenital heart disease
    Prince J Kannankeril
    Department of Medicine, Vanderbilty University Medical Center, Nashville, Tennessee 37232 2572, USA
    Am J Cardiol 92:879-81. 2003
    ..Of the 23 patients who were free of recurrence 1 year after ablation, 21 (91%) remain free from recurrence at an average of 45 months (median 39; range 15 to 88) after ablation...
  11. ncbi request reprint Temporal changes in ventricular function assessed echocardiographically in conscious and anesthetized mice
    Jeffrey N Rottman
    Department of Internal Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232 6300, USA
    J Am Soc Echocardiogr 16:1150-7. 2003
    ..Serial echocardiographic assessments of cardiac function, dimension, and mass can be performed with high reproducibility in conscious mice...
  12. ncbi request reprint Potassium current antagonist properties and proarrhythmic consequences of quinolone antibiotics
    M E Anderson
    Vanderbilt University Medical Center, Department of Internal Medicine and Pharmacology, Divisions of Clinical Pharmacology and Cardiovascular Medicine, Nashville, Tennessee 37232 6300, USA
    J Pharmacol Exp Ther 296:806-10. 2001
    ..These findings show that I(Kr) block may be a common feature of many quinolone antibiotics, and that the proarrhythmic consequences vary according to I(Kr) antagonist potency, but are also influenced by additional, unidentified factors...
  13. ncbi request reprint Replacement by homologous recombination of the minK gene with lacZ reveals restriction of minK expression to the mouse cardiac conduction system
    S Kupershmidt
    Departments of Medicine Pharmacology, Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN, USA
    Circ Res 84:146-52. 1999
    ..More generally, the restricted nature of minK expression in the mouse heart suggests species-specific roles of this gene product in mediating the electrophysiological properties of the heart...
  14. pmc A β(IV)-spectrin/CaMKII signaling complex is essential for membrane excitability in mice
    Thomas J Hund
    Department of Internal Medicine, Division of Cardiovascular Medicine, University of Iowa Carver College of Medicine, Iowa City, Iowa 52242, USA
    J Clin Invest 120:3508-19. 2010
    ..Collectively, our data define an unexpected but indispensable molecular platform that determines membrane excitability in the mouse heart and brain...
  15. ncbi request reprint Reduced repolarization reserve in ventricular myocytes from female mice
    Yuejin Wu
    Department of Medicine, 315 Preston Research Building II, Vanderbilt University Medical Center, Nashville, TN 37232 6300, USA
    Cardiovasc Res 53:763-9. 2002
    ..Mice are an increasingly important experimental model animal for cardiovascular research, but gender-dependent differences have not been reported for repolarization in murine ventricular myocytes...
  16. pmc Proarrhythmic defects in Timothy syndrome require calmodulin kinase II
    William H Thiel
    Vanderbilt University, Nashville, TN, USA
    Circulation 118:2225-34. 2008
    ..2 current (I(Ca)). During cellular Ca(2+) overload, the calmodulin-dependent protein kinase II (CaMKII) causes arrhythmias. We hypothesized that CaMKII is a part of the proarrhythmic mechanism in TS...
  17. pmc Calmodulin kinase is functionally targeted to the action potential plateau for regulation of L-type Ca2+ current in rabbit cardiomyocytes
    Yuejin Wu
    Department of Internal Medicine, Vanderbilt University Medical Center, Nashville, TN 37232 6300, USA
    J Physiol 554:145-55. 2004
    ..These findings show that ICa-L responses to CaMK are voltage dependent and suggest a new model of L-type Ca2+ channel regulation where voltage-dependent changes control ICa-L responses to Ca2+-CaM and CaMK signalling...
  18. pmc Calmodulin kinase and a calmodulin-binding 'IQ' domain facilitate L-type Ca2+ current in rabbit ventricular myocytes by a common mechanism
    Y Wu
    Department of Internal Medicine, Vanderbilt University, Nashville, TN 37232-6300, USA
    J Physiol 535:679-87. 2001
    ..Both CaMK and IQmp were able to induce a modal gating shift in LTCCs, suggesting that each of these signalling elements is important for Ca2+-CaM-dependent LTCC facilitation in cardiac myocytes...
  19. ncbi request reprint Ca2+-dependent regulation of cardiac L-type Ca2+ channels: is a unifying mechanism at hand?
    M E Anderson
    Department of Internal Medicine, Vanderbilt University, Nashville, Tennessee 37232, USA
    J Mol Cell Cardiol 33:639-50. 2001
    ..A recent explosion of work has shed new light on the mechanisms and molecular identity of domains necessary for [Ca2+]i-dependent regulation of LTCC...
  20. ncbi request reprint Calmodulin kinase II inhibition protects against structural heart disease
    Rong Zhang
    Department of Medicine, Vanderbilt University School of Medicine, 2220 Pierce Avenue, Nashville, Tennessee 37232 6300, USA
    Nat Med 11:409-17. 2005
    ..These findings mark CaMKII as a determinant of clinically important heart disease phenotypes, and suggest CaMKII inhibition can be a highly selective approach for targeting adverse myocardial remodeling linked to betaAR signaling...
  21. ncbi request reprint Atrial fibrillation in KCNE1-null mice
    Joel Temple
    Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tenn 37232 6602, USA
    Circ Res 97:62-9. 2005
    ..Thus, KCNE1 deletion in mice unexpectedly leads to increased outward current in atrial myocytes, shortens atrial action potentials, and enhances susceptibility to atrial fibrillation...
  22. ncbi request reprint An EF-hand in the sodium channel couples intracellular calcium to cardiac excitability
    Tammy L Wingo
    Department of Pharmacology, Vanderbilt University, Nashville, Tennessee 37232, USA
    Nat Struct Mol Biol 11:219-25. 2004
    ..These studies reveal the molecular basis for certain forms of long QT syndrome and other arrhythmia-producing syndromes, and suggest a potential pharmacological target for antiarrhythmic drug design...
  23. ncbi request reprint Death, cardiac dysfunction, and arrhythmias are increased by calmodulin kinase II in calcineurin cardiomyopathy
    Michelle S C Khoo
    Department of Medicine, Vanderbilt University, Nashville, Tenn, USA
    Circulation 114:1352-9. 2006
    ....
  24. pmc C terminus L-type Ca2+ channel calmodulin-binding domains are 'auto-agonist' ligands in rabbit ventricular myocytes
    Igor Dzhura
    Department of Internal Medicine, Vanderbilt University, Nashville, TN 37232, USA
    J Physiol 550:731-8. 2003
    ..CBmp and CaMKII increased L-type Ca2+ channel Po in a non-additive manner, suggesting that low and high Ca(2+)-CaM-dependent L-type Ca2+ channel facilitation pathways converge upon a common signalling mechanism...
  25. ncbi request reprint CaMKII, an emerging molecular driver for calcium homeostasis, arrhythmias, and cardiac dysfunction
    Chad E Grueter
    Department of Molecular Physiology and Biophysics, Vanderbilt University Medical Center, Nashville, TN, USA
    J Mol Med (Berl) 85:5-14. 2007
    ..Moreover, CaMKII was recently identified as a potential drug target in cardiac disease. This work has given us a closer view of the complexity and therapeutic possibilities of CaMKII regulation of Ca(2+) signaling in cardiac myocytes...
  26. ncbi request reprint A dynamic alpha-beta inter-subunit agonist signaling complex is a novel feedback mechanism for regulating L-type Ca2+ channel opening
    Rong Zhang
    Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA
    FASEB J 19:1573-5. 2005
    ..Thus, the bifunctional ability of the alpha subunit CaM binding motifs to competitively associate with the beta subunit or CaM provides a novel paradigm for feedback control of cellular Ca2+ entry...
  27. pmc Mice with the R176Q cardiac ryanodine receptor mutation exhibit catecholamine-induced ventricular tachycardia and cardiomyopathy
    Prince J Kannankeril
    Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, TN 37232, USA
    Proc Natl Acad Sci U S A 103:12179-84. 2006
    ..Our results suggest that the R176Q mutation in RyR2 predisposes the heart to catecholamine-induced oscillatory calcium-release events that trigger a calcium-dependent ventricular arrhythmia...
  28. ncbi request reprint Calmodulin kinase II inhibition protects against myocardial cell apoptosis in vivo
    Yingbo Yang
    Dept of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA
    Am J Physiol Heart Circ Physiol 291:H3065-75. 2006
    ..These findings indicate CaMKII is proapoptotic in vivo and suggest that regulation of SR Ca(2+) content by PLN contributes to the antiapoptotic mechanism of CaMKII inhibition...
  29. pmc Local control of Ca2+-induced Ca2+ release in mouse sinoatrial node cells
    Biyi Chen
    Division of Cardiovascular Medicine, Department of Internal Medicine, University of Iowa Carver College of Medicine, 285 Newton Road, Iowa City, IA 52242, USA
    J Mol Cell Cardiol 47:706-15. 2009
    ..We concluded that the "local control" mechanism of CICR is responsible for both local Ca2+ release during diastolic depolarization and the synchronized Ca2+ transients observed during action potential in SAN cells...
  30. ncbi request reprint Oxidative mediated lipid peroxidation recapitulates proarrhythmic effects on cardiac sodium channels
    Koji Fukuda
    Department of Anesthesiology, Vanderbilt University School of Medicine, Nashville, TN, USA
    Circ Res 97:1262-9. 2005
    ..These data suggest Na+ channel dysfunction evoked by lipid peroxidation is a candidate mechanism for ischemia-related conduction abnormalities and arrhythmias...
  31. ncbi request reprint Polymorphic ventricular tachycardia and abnormal Ca2+ handling in very-long-chain acyl-CoA dehydrogenase null mice
    Andreas A Werdich
    Division of Cardiology, Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, TN 37232 0001, USA
    Am J Physiol Heart Circ Physiol 292:H2202-11. 2007
    ..We conclude that intracellular Ca(2+) handling represents a possible molecular mechanism of arrhythmias in mice and perhaps in VLCAD-deficient humans...
  32. pmc Cytoskeletal disrupting agents prevent calmodulin kinase, IQ domain and voltage-dependent facilitation of L-type Ca2+ channels
    Igor Dzhura
    Department of Internal Medicine, Vanderbilt University Medical Center, Vanderbilt University, Nashville, TN 37232 6300, USA
    J Physiol 545:399-406. 2002
    ....
  33. ncbi request reprint Pause-dependent polymorphic ventricular tachycardia during long-term treatment with dofetilide: a placebo-controlled, implantable cardioverter-defibrillator-based evaluation
    A Mazur
    Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA
    J Am Coll Cardiol 37:1100-5. 2001
    ..These data suggest that in ICD patients either long-term dofetilide therapy is associated with an increased risk of TdP or the drug alters VT morphology...
  34. ncbi request reprint Functional similarity between electrograms recorded from an implantable cardioverter defibrillator emulator and the surface electrocardiogram
    A Mazur
    Vanderbilt University Medical Center, Nashville, Tennessee 37232-6300, USA
    Pacing Clin Electrophysiol 24:34-40. 2001
    ..They also may be useful as a surrogate of the ECG for analysis and monitoring of different components of P-QRS-T complex...
  35. ncbi request reprint L-type Ca2+ channel facilitation mediated by phosphorylation of the beta subunit by CaMKII
    Chad E Grueter
    Department of Molecular Physiology and Biophysics, Vanderbilt University Medical Center, Nashville, Tennessee 37232, USA
    Mol Cell 23:641-50. 2006
    ..These findings reveal a molecular mechanism for targeting CaMKII to LTCCs and facilitating I(Ca) that may modulate Ca(2+) entry in diverse cell types coexpressing CaMKII and the beta(2a) subunit...
  36. doi request reprint The role of calmodulin kinase II in myocardial physiology and disease
    Luis F Couchonnal
    Departments of Internal Medicine, Division of Cardiovascular Medicine, University of Iowa, Carver College of Medicine, Iowa City, Iowa, USA
    Physiology (Bethesda) 23:151-9. 2008
    ..Under stress conditions, excessive CaMKII activity promotes heart failure and arrhythmias, in part through actions at Ca(2+) homeostatic proteins. Here, we briefly review the molecular and cellular physiology of CaMKII in myocardium...
  37. pmc Ca2+/calmodulin-dependent kinase II triggers cell membrane injury by inducing complement factor B gene expression in the mouse heart
    Madhu V Singh
    Division of Cardiovascular Medicine, Carver College of Medicine, University of Iowa, Iowa City, Iowa 52242, USA
    J Clin Invest 119:986-96. 2009
    ..Our findings demonstrate what we believe is a novel target for CaMKII in myocardial injury and suggest that CaMKII is broadly important for the genetic effects of MI in cardiomyocytes...
  38. pmc Ankyrin-B regulates Kir6.2 membrane expression and function in heart
    Jingdong Li
    Division of Cardiovascular Medicine, Department of Internal Medicine, University of Iowa Carver College of Medicine, Iowa City, Iowa 52242, USA
    J Biol Chem 285:28723-30. 2010
    ..Collectively, our new findings define a new role for cardiac ankyrin polypeptides in regulation of ion channel membrane expression in heart...
  39. pmc Differential regulated interactions of calcium/calmodulin-dependent protein kinase II with isoforms of voltage-gated calcium channel beta subunits
    Chad E Grueter
    Department of Molecular Physiology and Biophysics, Vanderbilt University Medical Center, Nashville, Tennessee 37232, USA
    Biochemistry 47:1760-7. 2008
    ..In combination, these data show that phosphorylation dynamically regulates the interactions of specific isoforms of the Ca2+ channel beta subunits with CaMKII...
  40. ncbi request reprint Reduced contractile response to alpha1-adrenergic stimulation in atria from mice with chronic cardiac calmodulin kinase II inhibition
    Michael Grimm
    Institute of Experimental and Clinical Pharmacology and Toxicology, University Medical Center Hamburg Eppendorf, Hamburg, Germany
    J Mol Cell Cardiol 42:643-52. 2007
    ..Our data indicate a role of CaMKII in post-rest potentiation and the positive inotropic effect of alpha-adrenergic stimulation at low frequencies...
  41. ncbi request reprint A calcium sensor in the sodium channel modulates cardiac excitability
    Hanno L Tan
    Department of Anesthesiology, Vanderbilt University School of Medicine, Nashville 37232, Tennessee, USA
    Nature 415:442-7. 2002
    ....
  42. ncbi request reprint "We are not alone": ion channel mutations in a long QT syndrome cohort
    Mark E Anderson
    Heart Rhythm 2:1106-7. 2005
  43. ncbi request reprint Multiple downstream proarrhythmic targets for calmodulin kinase II: moving beyond an ion channel-centric focus
    Mark E Anderson
    University of Iowa, Carver College of Medicine, Department of Internal Medicine, 200 Hawkins Drive, E315 A1 GH, Iowa City, IA 52242 USA
    Cardiovasc Res 73:657-66. 2007
    ....
  44. ncbi request reprint Calmodulin kinase II inhibition shortens action potential duration by upregulation of K+ currents
    Jingdong Li
    Department of Internal Medicine, University of Iowa, Carver College of Medicine, Iowa City, USA
    Circ Res 99:1092-9. 2006
    ..These findings provide novel in vivo and cellular evidence that CaMKII links Ca(2+)(i) to cardiac repolarization and suggest that PLN may be a critical CaMKII target for feedback regulation of APD in ventricular myocytes...
  45. ncbi request reprint The fire from within: the biggest Ca2+ channel erupts and dribbles
    Mark E Anderson
    Circ Res 97:1213-5. 2005
  46. ncbi request reprint Deciphering the message of long QT genotypes
    John T Kimbrough
    J Cardiovasc Electrophysiol 14:1154-5. 2003
  47. ncbi request reprint Calcium and stunning: when, from where, and what next?
    Mark E Anderson
    J Cardiovasc Electrophysiol 13:1025-6. 2002
  48. ncbi request reprint Suppression of dynamic Ca(2+) transient responses to pacing in ventricular myocytes from mice with genetic calmodulin kinase II inhibition
    Yuejin Wu
    Department of Internal Medicine, Vanderbilt University
    J Mol Cell Cardiol 40:213-23. 2006
    ..These findings show that chronic CaMKII inhibition reduces variability of CICR responses in a manner that is partly dependent on the presence of PLN...
  49. ncbi request reprint Too little, too late: chasing atrial fibrillation with sodium channel antagonists
    Mark E Anderson
    J Cardiovasc Electrophysiol 17:655-6. 2006
  50. pmc Sudden Infant Death Syndrome and prenatal maternal smoking: rising attributed risk in the Back to Sleep era
    Mark E Anderson
    Department of Community Health Services, Division of Pediatrics, Denver Health and Hospitals Authority, Denver, Colorado, USA
    BMC Med 3:4. 2005
    ..This study quantifies the relationship between prenatal smoking and infant death over the time period of the Back to Sleep campaign in the United States, which encouraged parents to use a supine sleeping position for infants...
  51. ncbi request reprint Calmodulin kinase II inhibition enhances ischemic preconditioning by augmenting ATP-sensitive K+ current
    Jingdong Li
    Departments of Medicine, Carver College of Medicine, University of Iowa, Iowa City, Iowa 52242 1081, USA
    Channels (Austin) 1:387-94. 2007
    ..Our study results show CaMKII inhibition enhances beneficial effects of IP by increasing I(KATP)...
  52. ncbi request reprint Successful school-based intervention for inner-city children with persistent asthma
    Mark E Anderson
    Department of Community Health Services, Denver Health, Denver, Colorado 80204, USA
    J Asthma 41:445-53. 2004
    ..This study sought to determine the impact of the Kunsberg program on asthma utilization...
  53. ncbi request reprint Disease mechanisms and emerging therapies: protein kinases and their inhibitors in myocardial disease
    Mark E Anderson
    Cardiovascular Research Center at the University of Iowa, Iowa City 52242 1081, USA
    Nat Clin Pract Cardiovasc Med 3:437-45. 2006
    ....
  54. pmc Calmodulin kinase II inhibition disrupts cardiomyopathic effects of enhanced green fluorescent protein
    Michelle S C Khoo
    Department of Internal Medicine, University of Colorado at Denver and Health Sciences Center, Aurora, CO 80045, USA
    J Mol Cell Cardiol 44:405-10. 2008
    ..These findings suggest that increased CaMKII activity is a critical pathological signal in transgenic cardiomyopathy due to eGFP over-expression...
  55. ncbi request reprint When will we know enough to treat atrial fibrillation?
    Mark E Anderson
    Heart Rhythm 4:750-1. 2007
  56. ncbi request reprint MicroRNA may have macro effect on sudden death
    Mark E Anderson
    Nat Med 13:410-1. 2007
  57. pmc A dynamic pathway for calcium-independent activation of CaMKII by methionine oxidation
    Jeffrey R Erickson
    Department of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, IA 52242 1109, USA
    Cell 133:462-74. 2008
    ..Our data demonstrate a dynamic mechanism for CaMKII activation by oxidation and highlight the critical importance of oxidation-dependent CaMKII activation to AngII and ischemic myocardial apoptosis...