Jingsong Zhou

Summary

Affiliation: Rush University Medical Center
Country: USA

Publications

  1. pmc Hyperactive intracellular calcium signaling associated with localized mitochondrial defects in skeletal muscle of an animal model of amyotrophic lateral sclerosis
    Jingsong Zhou
    Department of Molecular Biophysics and Physiology, Rush University Medical School, Chicago, Illinois 60612, USA
    J Biol Chem 285:705-12. 2010
  2. ncbi request reprint A probable role of dihydropyridine receptors in repression of Ca2+ sparks demonstrated in cultured mammalian muscle
    Jingsong Zhou
    Section of Cellular Signaling, Department of Molecular Biophysics and Physiology, Rush University, Chicago 60612, USA
    Am J Physiol Cell Physiol 290:C539-53. 2006
  3. pmc Measurement of RyR permeability reveals a role of calsequestrin in termination of SR Ca(2+) release in skeletal muscle
    Monika Sztretye
    Section of Cellular Signaling, Department of Molecular Biophysics and Physiology, Rush University, Chicago, IL 60612, USA
    J Gen Physiol 138:231-47. 2011
  4. pmc The changes in Ca2+ sparks associated with measured modifications of intra-store Ca2+ concentration in skeletal muscle
    Bradley S Launikonis
    Section of Cellular Signaling, Department of Molecular Biophysics and Physiology, Rush University, Chicago, IL 60612, USA
    J Gen Physiol 128:45-54. 2006
  5. pmc Paradoxical buffering of calcium by calsequestrin demonstrated for the calcium store of skeletal muscle
    Leandro Royer
    Section of Cellular Signaling, Department of Molecular Biophysics and Physiology, Rush University, Chicago, IL 60612, USA
    J Gen Physiol 136:325-38. 2010
  6. pmc Ca(2+) sparks operated by membrane depolarization require isoform 3 ryanodine receptor channels in skeletal muscle
    Sandrine Pouvreau
    Section of Cellular Signaling, Department of Molecular Biophysics and Physiology, Rush University, 1750 West Harrison Street, Suite 1279JS, Chicago, IL 60612, USA
    Proc Natl Acad Sci U S A 104:5235-40. 2007
  7. pmc Calcium-dependent inactivation terminates calcium release in skeletal muscle of amphibians
    Eduardo Rios
    Section of Cellular Signaling, Department of Molecular Biophysics and Physiology, Rush University, Chicago, IL 60612, USA
    J Gen Physiol 131:335-48. 2008
  8. pmc Depletion "skraps" and dynamic buffering inside the cellular calcium store
    Bradley S Launikonis
    Section of Cellular Signaling, Department of Molecular Biophysics and Physiology, Rush University, 1750 West Harrison Street, Suite 1279JS, Chicago, IL 60612, USA
    Proc Natl Acad Sci U S A 103:2982-7. 2006
  9. pmc Altered Ca2+ concentration, permeability and buffering in the myofibre Ca2+ store of a mouse model of malignant hyperthermia
    Carlo Manno
    S L Hamilton E Ríos Rush University School of Medicine, Department of Molecular Biophysics and Physiology, 1750 West Harrison St, Suite 1279JS, Chicago, IL 60612, USA Email
    J Physiol 591:4439-57. 2013
  10. pmc Regulation of Ca2+ sparks by Ca2+ and Mg2+ in mammalian and amphibian muscle. An RyR isoform-specific role in excitation-contraction coupling?
    Jingsong Zhou
    Department of Molecular Biophysics and Physiology, Rush University, Chicago, IL 60612, USA
    J Gen Physiol 124:409-28. 2004

Collaborators

Detail Information

Publications18

  1. pmc Hyperactive intracellular calcium signaling associated with localized mitochondrial defects in skeletal muscle of an animal model of amyotrophic lateral sclerosis
    Jingsong Zhou
    Department of Molecular Biophysics and Physiology, Rush University Medical School, Chicago, Illinois 60612, USA
    J Biol Chem 285:705-12. 2010
    ..Our data reveal that mitochondria regulate Ca(2+) signaling in skeletal muscle, and loss of this capacity may contribute to the progression of muscle atrophy in ALS...
  2. ncbi request reprint A probable role of dihydropyridine receptors in repression of Ca2+ sparks demonstrated in cultured mammalian muscle
    Jingsong Zhou
    Section of Cellular Signaling, Department of Molecular Biophysics and Physiology, Rush University, Chicago 60612, USA
    Am J Physiol Cell Physiol 290:C539-53. 2006
    ..These data suggest that DHPRs play a critical role in reducing the rate of spontaneous opening of Ca(2+) release channels and/or their susceptibility to Ca(2+)-induced activation, thereby suppressing the production of Ca(2+) sparks...
  3. pmc Measurement of RyR permeability reveals a role of calsequestrin in termination of SR Ca(2+) release in skeletal muscle
    Monika Sztretye
    Section of Cellular Signaling, Department of Molecular Biophysics and Physiology, Rush University, Chicago, IL 60612, USA
    J Gen Physiol 138:231-47. 2011
    ..This observation indicates that [Ca(2+)](SR), sensed by Casq and transmitted to the channels presumably via connecting proteins, is determinant to cause the closure that terminates Ca(2+) release...
  4. pmc The changes in Ca2+ sparks associated with measured modifications of intra-store Ca2+ concentration in skeletal muscle
    Bradley S Launikonis
    Section of Cellular Signaling, Department of Molecular Biophysics and Physiology, Rush University, Chicago, IL 60612, USA
    J Gen Physiol 128:45-54. 2006
    ....
  5. pmc Paradoxical buffering of calcium by calsequestrin demonstrated for the calcium store of skeletal muscle
    Leandro Royer
    Section of Cellular Signaling, Department of Molecular Biophysics and Physiology, Rush University, Chicago, IL 60612, USA
    J Gen Physiol 136:325-38. 2010
    ..The study revealed a surprisingly modest loss of Ca(2+) storage capacity in null cells, which may reflect concurrent changes, rather than detract from the physiological importance of calsequestrin...
  6. pmc Ca(2+) sparks operated by membrane depolarization require isoform 3 ryanodine receptor channels in skeletal muscle
    Sandrine Pouvreau
    Section of Cellular Signaling, Department of Molecular Biophysics and Physiology, Rush University, 1750 West Harrison Street, Suite 1279JS, Chicago, IL 60612, USA
    Proc Natl Acad Sci U S A 104:5235-40. 2007
    ..Physiologically voltage-controlled Ca(2+) sparks thus require a voltage sensor, a master junctional RyR1 channel that provides trigger Ca(2+), and a slave parajunctional RyR3 cohort...
  7. pmc Calcium-dependent inactivation terminates calcium release in skeletal muscle of amphibians
    Eduardo Rios
    Section of Cellular Signaling, Department of Molecular Biophysics and Physiology, Rush University, Chicago, IL 60612, USA
    J Gen Physiol 131:335-48. 2008
    ..Trivially, an inverse proportionality between release flux and duration, in sparks or in global release of skeletal muscle, maintains constancy of the amount of released Ca2+...
  8. pmc Depletion "skraps" and dynamic buffering inside the cellular calcium store
    Bradley S Launikonis
    Section of Cellular Signaling, Department of Molecular Biophysics and Physiology, Rush University, 1750 West Harrison Street, Suite 1279JS, Chicago, IL 60612, USA
    Proc Natl Acad Sci U S A 103:2982-7. 2006
    ..When store depletion becomes widespread, the polymers would collapse to increase store [Ca2+] and sustain the concentration gradient that drives release flux...
  9. pmc Altered Ca2+ concentration, permeability and buffering in the myofibre Ca2+ store of a mouse model of malignant hyperthermia
    Carlo Manno
    S L Hamilton E Ríos Rush University School of Medicine, Department of Molecular Biophysics and Physiology, 1750 West Harrison St, Suite 1279JS, Chicago, IL 60612, USA Email
    J Physiol 591:4439-57. 2013
    ..The unstable SR buffering, mimicked by silencing of calsequestrin, may help precipitate the loss of Ca2+ control that defines a fulminant MH event...
  10. pmc Regulation of Ca2+ sparks by Ca2+ and Mg2+ in mammalian and amphibian muscle. An RyR isoform-specific role in excitation-contraction coupling?
    Jingsong Zhou
    Department of Molecular Biophysics and Physiology, Rush University, Chicago, IL 60612, USA
    J Gen Physiol 124:409-28. 2004
    ..It is proposed that relief of this inhibition could be the mechanism by which increased SR load increases spark frequency...
  11. pmc Synthetic localized calcium transients directly probe signalling mechanisms in skeletal muscle
    Lourdes Figueroa
    Section of Cellular Signaling, Department of Molecular Biophysics and Physiology, Rush University School of Medicine, 1750 W Harrison St, Suite 1279JS, Chicago, IL 60612, USA
    J Physiol 590:1389-411. 2012
    ..The differences in flux and threshold may be ascribed to the absence of ryanodine receptor 3 (RyR3) isoforms in adult mammalian muscle...
  12. pmc D4cpv-calsequestrin: a sensitive ratiometric biosensor accurately targeted to the calcium store of skeletal muscle
    Monika Sztretye
    Section of Cellular Signaling, Department of Molecular Biophysics and Physiology, Rush University, Chicago, IL 60612, USA
    J Gen Physiol 138:211-29. 2011
    ..It is demonstrably small in D4cpv. D4cpv-Casq1 therefore provides substantial improvements in sensitivity, specificity, and reproducibility over existing monitors of SR free Ca(2+) concentration...
  13. pmc Confocal imaging of [Ca2+] in cellular organelles by SEER, shifted excitation and emission ratioing of fluorescence
    Bradley S Launikonis
    Section of Cellular Signaling, Department of Molecular Biophysics and Physiology, Rush University School of Medicine, 1750 W Harrison St Suite 1279JS, Chicago, IL 60612, USA
    J Physiol 567:523-43. 2005
    ..While the increase of [Ca2+]SR was limited by loss through Ca2+ release channels, its decrease in low [Ca2+]cyto was largely dependent on leaks through the SR Ca2+ pump...
  14. ncbi request reprint Control of dual isoforms of Ca2+ release channels in muscle
    Eduardo Rios
    Section of Cellular Signaling, Department of Molecular Biophysics and Physiology, Rush University, Chicago, IL 60612, USA
    Biol Res 37:583-91. 2004
    ..Several issues regarding the roles of different channels remain open to further study...
  15. pmc Mitochondrial calcium uptake regulates rapid calcium transients in skeletal muscle during excitation-contraction (E-C) coupling
    Jianxun Yi
    Department of Molecular Biophysics and Physiology, Rush University School of Medicine, Chicago, Illinois 60612, USA
    J Biol Chem 286:32436-43. 2011
    ....
  16. pmc Defective mitochondrial dynamics is an early event in skeletal muscle of an amyotrophic lateral sclerosis mouse model
    Guo Luo
    Department of Molecular Biophysics and Physiology, Rush University School of Medicine, Chicago, Illinois, United States of America Zunyi Medical College, Zunyi, China
    PLoS ONE 8:e82112. 2013
    ....
  17. ncbi request reprint Uncontrolled calcium sparks act as a dystrophic signal for mammalian skeletal muscle
    Xu Wang
    Department of Physiology and Biophysics, UMDNJ Robert Wood Johnson Medical School, 675 Hoes Lane, Piscataway, NJ 08854, USA
    Nat Cell Biol 7:525-30. 2005
    ....
  18. ncbi request reprint Phosphorylation and putative ER retention signals are required for protein kinase A-mediated potentiation of cardiac sodium current
    Jingsong Zhou
    Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tenn 37232 6602, USA
    Circ Res 91:540-6. 2002
    ....