Mark S Miller

Summary

Affiliation: University of Vermont
Country: USA

Publications

  1. pmc Aging enhances indirect flight muscle fiber performance yet decreases flight ability in Drosophila
    Mark S Miller
    Department of Molecular Physiology and Biophysics, University of Vermont, Burlington, Vermont 05405, USA
    Biophys J 95:2391-401. 2008
  2. ncbi request reprint The essential light chain N-terminal extension alters force and fiber kinetics in mouse cardiac muscle
    Mark S Miller
    Department of Molecular Physiology and Biophysics, University of Vermont, Burlington, Vermont 05405, USA
    J Biol Chem 280:34427-34. 2005
  3. pmc Age-related slowing of myosin actin cross-bridge kinetics is sex specific and predicts decrements in whole skeletal muscle performance in humans
    Mark S Miller
    Department of Molecular Physiology and Biophysics, University of Vermont, College of Medicine, Burlington, Vermont
    J Appl Physiol (1985) 115:1004-14. 2013
  4. pmc Thick-to-thin filament surface distance modulates cross-bridge kinetics in Drosophila flight muscle
    Bertrand C W Tanner
    Department of Molecular Physiology and Biophysics, University of Vermont, Burlington, Vermont, USA
    Biophys J 103:1275-84. 2012
  5. pmc Alternative S2 hinge regions of the myosin rod affect myofibrillar structure and myosin kinetics
    Mark S Miller
    Department of Molecular Physiology and Biophysics, University of Vermont, Burlington, Vermont, USA
    Biophys J 96:4132-43. 2009
  6. pmc Mechanisms underlying skeletal muscle weakness in human heart failure: alterations in single fiber myosin protein content and function
    Mark S Miller
    Departments of Molecular Physiology and Biophysics and Medicine, University of Vermont, College of Medicine, Burlington, VT, USA
    Circ Heart Fail 2:700-6. 2009
  7. pmc COOH-terminal truncation of flightin decreases myofilament lattice organization, cross-bridge binding, and power output in Drosophila indirect flight muscle
    Bertrand C W Tanner
    Department of Molecular Physiology and Biophysics, University of Vermont, Burlington, VT 05405, USA
    Am J Physiol Cell Physiol 301:C383-91. 2011
  8. pmc Effect of resistance training on physical disability in chronic heart failure
    Patrick A Savage
    Department of Medicine, College of Medicine, University of Vermont, Burlington, VT 05405, USA
    Med Sci Sports Exerc 43:1379-86. 2011
  9. pmc Regulatory light chain phosphorylation and N-terminal extension increase cross-bridge binding and power output in Drosophila at in vivo myofilament lattice spacing
    Mark S Miller
    Department of Molecular Physiology and Biophysics, University of Vermont, Burlington, Vermont, USA
    Biophys J 100:1737-46. 2011
  10. pmc Molecular mechanisms underlying skeletal muscle weakness in human cancer: reduced myosin-actin cross-bridge formation and kinetics
    Michael J Toth
    Department of Medicine, University of Vermont, College of Medicine, Burlington, VT, USA
    J Appl Physiol (1985) 114:858-68. 2013

Collaborators

Detail Information

Publications27

  1. pmc Aging enhances indirect flight muscle fiber performance yet decreases flight ability in Drosophila
    Mark S Miller
    Department of Molecular Physiology and Biophysics, University of Vermont, Burlington, Vermont 05405, USA
    Biophys J 95:2391-401. 2008
    ..We also speculate that a lack of MgATP due to damaged mitochondria accounts for the decreased flight performance...
  2. ncbi request reprint The essential light chain N-terminal extension alters force and fiber kinetics in mouse cardiac muscle
    Mark S Miller
    Department of Molecular Physiology and Biophysics, University of Vermont, Burlington, Vermont 05405, USA
    J Biol Chem 280:34427-34. 2005
    ..Our results strongly suggest that an interaction between residues 5-14 of the ELC N terminus and the C-terminal residues of actin enhances cardiac performance...
  3. pmc Age-related slowing of myosin actin cross-bridge kinetics is sex specific and predicts decrements in whole skeletal muscle performance in humans
    Mark S Miller
    Department of Molecular Physiology and Biophysics, University of Vermont, College of Medicine, Burlington, Vermont
    J Appl Physiol (1985) 115:1004-14. 2013
    ..Thus these results support our hypothesis that age-related alterations in the myosin molecule contribute to skeletal muscle dysfunction and physical disability and indicate that this effect is stronger in women. ..
  4. pmc Thick-to-thin filament surface distance modulates cross-bridge kinetics in Drosophila flight muscle
    Bertrand C W Tanner
    Department of Molecular Physiology and Biophysics, University of Vermont, Burlington, Vermont, USA
    Biophys J 103:1275-84. 2012
    ..Together, these structural changes may provide a mechanism for altering cross-bridge performance throughout a contraction-relaxation cycle...
  5. pmc Alternative S2 hinge regions of the myosin rod affect myofibrillar structure and myosin kinetics
    Mark S Miller
    Department of Molecular Physiology and Biophysics, University of Vermont, Burlington, Vermont, USA
    Biophys J 96:4132-43. 2009
    ..Our results indicate that this hinge region plays an important role in determining myosin kinetics and in regulating thick and thin filament lengths as well as sarcomere length...
  6. pmc Mechanisms underlying skeletal muscle weakness in human heart failure: alterations in single fiber myosin protein content and function
    Mark S Miller
    Departments of Molecular Physiology and Biophysics and Medicine, University of Vermont, College of Medicine, Burlington, VT, USA
    Circ Heart Fail 2:700-6. 2009
    ..Patients with chronic heart failure (HF) frequently experience skeletal muscle weakness that limits physical function. The mechanisms underlying muscle weakness, however, have not been clearly defined...
  7. pmc COOH-terminal truncation of flightin decreases myofilament lattice organization, cross-bridge binding, and power output in Drosophila indirect flight muscle
    Bertrand C W Tanner
    Department of Molecular Physiology and Biophysics, University of Vermont, Burlington, VT 05405, USA
    Am J Physiol Cell Physiol 301:C383-91. 2011
    ..These results indicate that the COOH terminus of flightin is necessary for normal myofilament lattice organization, thereby facilitating the cross-bridge binding required to achieve high power output for flight...
  8. pmc Effect of resistance training on physical disability in chronic heart failure
    Patrick A Savage
    Department of Medicine, College of Medicine, University of Vermont, Burlington, VT 05405, USA
    Med Sci Sports Exerc 43:1379-86. 2011
    ....
  9. pmc Regulatory light chain phosphorylation and N-terminal extension increase cross-bridge binding and power output in Drosophila at in vivo myofilament lattice spacing
    Mark S Miller
    Department of Molecular Physiology and Biophysics, University of Vermont, Burlington, Vermont, USA
    Biophys J 100:1737-46. 2011
    ....
  10. pmc Molecular mechanisms underlying skeletal muscle weakness in human cancer: reduced myosin-actin cross-bridge formation and kinetics
    Michael J Toth
    Department of Medicine, University of Vermont, College of Medicine, Burlington, VT, USA
    J Appl Physiol (1985) 114:858-68. 2013
    ..Collectively, our results suggest reductions in myofilament protein function as a potential molecular mechanism contributing to muscle weakness and physical disability in human cancer...
  11. pmc Two-state model of acto-myosin attachment-detachment predicts C-process of sinusoidal analysis
    Bradley M Palmer
    Department of Molecular Physiology and Biophysics, University of Vermont, Burlington, Vermont, USA
    Biophys J 93:760-9. 2007
    ..Experimental results from activated cardiac muscle examined at different temperatures and containing predominately alpha- or beta-myosin heavy chain isoforms were found to be consistent with the above interpretation...
  12. pmc Chronic heart failure decreases cross-bridge kinetics in single skeletal muscle fibres from humans
    Mark S Miller
    Department of Molecular Physiology, University of Vermont, Burlington, VT 05405, USA
    J Physiol 588:4039-53. 2010
    ..Additionally, we uncovered a unique kinetic property of MHC I fibres, a potential indication of two distinct populations of cross-bridges, which may have important physiological consequences...
  13. pmc An inverse power-law distribution of molecular bond lifetimes predicts fractional derivative viscoelasticity in biological tissue
    Bradley M Palmer
    Department of Molecular Physiology and Biophysics, University of Vermont, Burlington, VT, USA
    Biophys J 104:2540-52. 2013
    ....
  14. pmc Resistance training alters skeletal muscle structure and function in human heart failure: effects at the tissue, cellular and molecular levels
    Michael J Toth
    Health Science Research Facility 126B, 149 Beaumont Ave, University of Vermont, Burlington, VT 05405, USA
    J Physiol 590:1243-59. 2012
    ..More broadly, these data highlight novel cellular and molecular adaptations in muscle structure and function that contribute to the resistance-trained phenotype...
  15. pmc Comparative biomechanics of thick filaments and thin filaments with functional consequences for muscle contraction
    Mark S Miller
    Department of Molecular Physiology and Biophysics, University of Vermont, Burlington, VT 05405, USA
    J Biomed Biotechnol 2010:473423. 2010
    ..Here we review information on the material properties of thick filaments, thin filaments, and their primary constituents; we also discuss ways in which mechanical properties of filaments impact muscle performance...
  16. pmc Chronic heart failure reduces Akt phosphorylation in human skeletal muscle: relationship to muscle size and function
    Michael J Toth
    Health Science Research Facility, Univ of Vermont, Burlington, VT 05405, USA
    J Appl Physiol (1985) 110:892-900. 2011
    ..Because patients and controls were similar for age, muscle mass, and physical activity, we ascribe the observed alterations in Akt phosphorylation and its relationship to myosin protein content to the unique effects of the HF syndrome...
  17. ncbi request reprint Age-related structural alterations in human skeletal muscle fibers and mitochondria are sex specific: relationship to single-fiber function
    Damien M Callahan
    Department of Medicine, University of Vermont, Burlington, Vermont and
    J Appl Physiol (1985) 116:1582-92. 2014
    ....
  18. doi request reprint Myofilament protein alterations promote physical disability in aging and disease
    Mark S Miller
    Department of Molecular Physiology and Biophysics, University of Vermont, College of Medicine, Burlington, VT 05405, USA
    Exerc Sport Sci Rev 41:93-9. 2013
    ..Based on these data, we propose that age- and disease-related alterations in myofilament proteins represent one molecular mechanism contributing to the development of physical disability...
  19. pmc Reduced knee extensor function in heart failure is not explained by inactivity
    Michael J Toth
    Department of Medicine, University of Vermont, College of Medicine Burlington, VT 05405, United States
    Int J Cardiol 143:276-82. 2010
    ..The goal of this study was to determine if heart failure alters knee extensor muscle torque, power production or contractile velocity...
  20. pmc Skeletal muscle mitochondrial density, gene expression, and enzyme activities in human heart failure: minimal effects of the disease and resistance training
    Michael J Toth
    Department of Medicine, College of Medicine, University of Vermont, Burlington, VT, USA
    J Appl Physiol (1985) 112:1864-74. 2012
    ..Moreover, the beneficial effects of resistance training on physical function in HF patients and controls are likely not related to alterations in mitochondrial biology...
  21. pmc Distribution of myosin attachment times predicted from viscoelastic mechanics of striated muscle
    Bradley M Palmer
    Department of Molecular Physiology and Biophysics, University of Vermont, 122 HSRF, Beaumont Avenue, Burlington, VT 05405, USA
    J Biomed Biotechnol 2011:592343. 2011
    ....
  22. ncbi request reprint An infrared system for monitoring Drosophila motility during microgravity
    Mark S Miller
    Department of Mechanical Engineering, University of Vermont, Burlington, VT 05405, USA
    J Gravit Physiol 9:83-91. 2002
    ..DIMMS is also lightweight, compact, and power efficient. DIMMS has been flight tested onboard NASA's KC-135 reduced gravity research aircraft and a Nike-Orion sounding rocket...
  23. pmc Paramyosin phosphorylation site disruption affects indirect flight muscle stiffness and power generation in Drosophila melanogaster
    Hongjun Liu
    Department of Biology and Molecular Biology Institute, San Diego State University, 5500 Campanile Drive, San Diego, CA 92182 4614, USA
    Proc Natl Acad Sci U S A 102:10522-7. 2005
    ....
  24. ncbi request reprint Chlamydomonas IFT172 is encoded by FLA11, interacts with CrEB1, and regulates IFT at the flagellar tip
    Lotte B Pedersen
    Department of Molecular, Cellular, and Developmental Biology, Yale University, New Haven, CT 06520, USA
    Curr Biol 15:262-6. 2005
    ..Therefore, IFT172 is involved in the control of flagellar assembly/disassembly at the tip...
  25. ncbi request reprint Diphtheria toxin fused to variant interleukin-3 provides enhanced binding to the interleukin-3 receptor and more potent leukemia cell cytotoxicity
    Tie Fu Liu
    Department of Medicine and Cancer Biology, Wake Forest University School of Medicine, Winston Salem, NC, USA
    Exp Hematol 32:277-81. 2004
    ..One or both of these variant fusion proteins merit further development for therapy of chemotherapy refractory AML...
  26. pmc Passive stiffness in Drosophila indirect flight muscle reduced by disrupting paramyosin phosphorylation, but not by embryonic myosin S2 hinge substitution
    Yudong Hao
    Department of Bioengineering, University of Washington, Seattle, WA, USA
    Biophys J 91:4500-6. 2006
    ....
  27. pmc Spontaneous regression of advanced cancer: identification of a unique genetically determined, age-dependent trait in mice
    Zheng Cui
    Department of Pathology, Wake Forest University School of Medicine, Medical Center Boulevard, Winston Salem, NC 27157, USA
    Proc Natl Acad Sci U S A 100:6682-7. 2003
    ..The mice are healthy and cancer-free and have a normal life span. These observations suggest a previously unrecognized mechanism of immune surveillance, which may have potential for therapy or prevention of cancer...