Pre-assembled Ca2+ entry units and constitutively active Ca2+ entry in skeletal muscle of calsequestrin-1 knockout mice

Mice lacking calsequestrin-1 have reduced levels of releasable Ca2+ in the sarcoplasmic reticulum of their skeletal muscles. Michelucci et al. reveal that this is compensated by constitutive assembly of STIM1 and Orai1 into Ca2+ entry units, promoting both constitutive and store-operated Ca2+ entry.

[1]  J. Lawrence,et al.  Quantitative Measurement , 2021, Encyclopedia of Social Network Analysis and Mining.

[2]  T. Takano,et al.  Transverse tubule remodeling enhances Orai1-dependent Ca2+ entry in skeletal muscle , 2019, eLife.

[3]  A. Michelucci,et al.  Role of STIM1/ORAI1-mediated store-operated Ca2+ entry in skeletal muscle physiology and disease. , 2018, Cell calcium.

[4]  A. Michelucci,et al.  Addendum: Exercise-dependent formation of new junctions that promote STIM1-Orai1 assembly in skeletal muscle , 2018, Scientific Reports.

[5]  A. Michelucci,et al.  Aerobic Training Prevents Heatstrokes in Calsequestrin-1 Knockout Mice by Reducing Oxidative Stress , 2018, Oxidative medicine and cellular longevity.

[6]  M. Antal,et al.  SOCE Is Important for Maintaining Sarcoplasmic Calcium Content and Release in Skeletal Muscle Fibers. , 2017, Biophysical journal.

[7]  C. Reggiani,et al.  Identification and characterization of three novel mutations in the CASQ1 gene in four patients with tubular aggregate myopathy , 2017, Human mutation.

[8]  A. Michelucci,et al.  Exercise-dependent formation of new junctions that promote STIM1-Orai1 assembly in skeletal muscle , 2017, Scientific Reports.

[9]  A. Michelucci,et al.  Strenuous exercise triggers a life‐threatening response in mice susceptible to malignant hyperthermia , 2017, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[10]  R. Fitts,et al.  Calsequestrin depolymerizes when calcium is depleted in the sarcoplasmic reticulum of working muscle , 2017, Proceedings of the National Academy of Sciences.

[11]  S. Priori,et al.  Erratum: Role of the JP45-calsequestrin complex on calcium entry in slow twitch skeletal muscles (The Journal of Biological Chemistry (2016) 291, (14555-14565)) , 2016 .

[12]  S. Priori,et al.  Role of the JP45-calsequestrin complex on calcium entry in slow twitch skeletal muscles. , 2016, The Journal of Biological Chemistry.

[13]  H. McBride,et al.  Orai1 enhances muscle endurance by promoting fatigue‐resistant type I fiber content but not through acute store‐operated Ca2+ entry , 2016, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[14]  Dali Luo,et al.  Calsequestrin-1 Regulates Store-Operated Ca2+ Entry by Inhibiting STIM1 Aggregation , 2016, Cellular Physiology and Biochemistry.

[15]  S. Priori,et al.  Role of the JP45-Calsequestrin Complex on Calcium Entry in Slow Twitch Skeletal Muscles* , 2016, The Journal of Biological Chemistry.

[16]  A. Michelucci,et al.  Antioxidants Protect Calsequestrin-1 Knockout Mice from Halothane- and Heat-induced Sudden Death , 2015, Anesthesiology.

[17]  J. Putney,et al.  Retrograde regulation of STIM1-Orai1 interaction and store-operated Ca2+ entry by calsequestrin , 2015, Scientific Reports.

[18]  A. Michelucci,et al.  Oxidative stress, mitochondrial damage, and cores in muscle from calsequestrin-1 knockout mice , 2015, Skeletal Muscle.

[19]  S. Boncompagni,et al.  Orai1-dependent Calcium Entry Promotes Skeletal Muscle Growth and Limits Fatigue , 2013, Nature Communications.

[20]  F. Protasi,et al.  Accelerated Activation of SOCE Current in Myotubes from Two Mouse Models of Anesthetic- and Heat-Induced Sudden Death , 2013, PloS one.

[21]  E. Ríos,et al.  Altered Ca2+ concentration, permeability and buffering in the myofibre Ca2+ store of a mouse model of malignant hyperthermia , 2013, The Journal of physiology.

[22]  F. Protasi,et al.  Enhanced dihydropyridine receptor calcium channel activity restores muscle strength in JP45/CASQ1 double knockout mice , 2013, Nature Communications.

[23]  E. Finch,et al.  STIM1-Ca2+ Signaling Is Required for the Hypertrophic Growth of Skeletal Muscle in Mice , 2012, Molecular and Cellular Biology.

[24]  S. Boncompagni,et al.  Sequential stages in the age-dependent gradual formation and accumulation of tubular aggregates in fast twitch muscle fibers: SERCA and calsequestrin involvement , 2012, AGE.

[25]  E. Ríos,et al.  D4cpv-calsequestrin: a sensitive ratiometric biosensor accurately targeted to the calcium store of skeletal muscle , 2011, The Journal of general physiology.

[26]  E. Ríos,et al.  Measurement of RyR permeability reveals a role of calsequestrin in termination of SR Ca2+ release in skeletal muscle , 2011, The Journal of general physiology.

[27]  E. Ríos,et al.  Measurement of Intra-SR [Ca 2+] Reveals Changes in SR Ca 2+ Permeability During Intracellular Ca 2+ Release in Skeletal Muscle , 2011 .

[28]  G. Meissner,et al.  Muscle weakness in Ryr1I4895T/WT knock-in mice as a result of reduced ryanodine receptor Ca2+ ion permeation and release from the sarcoplasmic reticulum , 2011, The Journal of general physiology.

[29]  C. Reggiani,et al.  Massive alterations of sarcoplasmic reticulum free calcium in skeletal muscle fibers lacking calsequestrin revealed by a genetically encoded probe , 2010, Proceedings of the National Academy of Sciences.

[30]  C. Ward,et al.  Quantitative measurement of Ca²(+) in the sarcoplasmic reticulum lumen of mammalian skeletal muscle. , 2010, Biophysical journal.

[31]  D. H. Kim,et al.  Increased store-operated Ca2+ entry in skeletal muscle with reduced calsequestrin-1 expression. , 2010, Biophysical journal.

[32]  F. Protasi,et al.  Paradoxical buffering of calcium by calsequestrin demonstrated for the calcium store of skeletal muscle , 2010, The Journal of general physiology.

[33]  R. Dirksen Checking your SOCCs and feet: the molecular mechanisms of Ca2+ entry in skeletal muscle , 2009, The Journal of physiology.

[34]  F. Protasi,et al.  Calsequestrin‐1: a new candidate gene for malignant hyperthermia and exertional/environmental heat stroke , 2009, The Journal of physiology.

[35]  C. Reggiani,et al.  Anesthetic‐and heat‐induced sudden death in calsequestrin‐1‐knockout mice , 2009, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[36]  R. Dirksen,et al.  Differential dependence of store‐operated and excitation‐coupled Ca2+ entry in skeletal muscle on STIM1 and Orai1 , 2008, The Journal of physiology.

[37]  J. Eu,et al.  STIM1 signalling controls store-operated calcium entry required for development and contractile function in skeletal muscle , 2008, Nature Cell Biology.

[38]  C. Reggiani,et al.  Reorganized stores and impaired calcium handling in skeletal muscle of mice lacking calsequestrin‐1 , 2007, The Journal of physiology.

[39]  K. Fénelon,et al.  Role of calsequestrin evaluated from changes in free and total calcium concentrations in the sarcoplasmic reticulum of frog cut skeletal muscle fibres , 2007, The Journal of physiology.

[40]  Y. Gwack,et al.  Orai1 is an essential pore subunit of the CRAC channel , 2006, Nature.

[41]  Shenyuan L. Zhang,et al.  Molecular identification of the CRAC channel by altered ion selectivity in a mutant of Orai , 2006, Nature.

[42]  J. Kinet,et al.  CRACM1 Is a Plasma Membrane Protein Essential for Store-Operated Ca2+ Entry , 2006, Science.

[43]  Bogdan Tanasa,et al.  A mutation in Orai1 causes immune deficiency by abrogating CRAC channel function , 2006, Nature.

[44]  T. Deerinck,et al.  STIM1 is a Ca2+ sensor that activates CRAC channels and migrates from the Ca2+ store to the plasma membrane , 2005, Nature.

[45]  Tobias Meyer,et al.  STIM Is a Ca2+ Sensor Essential for Ca2+-Store-Depletion-Triggered Ca2+ Influx , 2005, Current Biology.

[46]  S. Wagner,et al.  STIM1, an essential and conserved component of store-operated Ca2+ channel function , 2005, The Journal of cell biology.

[47]  C. Caputo,et al.  Calcium transients in developing mouse skeletal muscle fibres , 2005, The Journal of physiology.

[48]  M. Hoth,et al.  Potent Inhibition of Ca2+ Release-activated Ca2+ Channels and T-lymphocyte Activation by the Pyrazole Derivative BTP2* , 2004, Journal of Biological Chemistry.

[49]  D. H. Kim,et al.  A Retrograde Signal from Calsequestrin for the Regulation of Store-operated Ca2+ Entry in Skeletal Muscle* , 2003, The Journal of Biological Chemistry.

[50]  Y. Ogawa,et al.  Depletion of Ca2+ in the sarcoplasmic reticulum stimulates Ca2+ entry into mouse skeletal muscle fibres , 2001, The Journal of physiology.

[51]  R. Steinhardt,et al.  A Capacitative Calcium Current in Cultured Skeletal Muscle Cells Is Mediated by the Calcium-specific Leak Channel and Inhibited by Dihydropyridine Compounds* , 1996, The Journal of Biological Chemistry.

[52]  Á. Zarain-Herzberg,et al.  Sarcoplasmic reticulum calsequestrins: Structural and functional properties , 1994, Molecular and Cellular Biochemistry.

[53]  K. Campbell,et al.  Purification and characterization of calsequestrin from canine cardiac sarcoplasmic reticulum and identification of the 53,000 dalton glycoprotein. , 1983, The Journal of biological chemistry.

[54]  B. Launikonis,et al.  Store‐operated Ca2+ entry is not required for store refilling in skeletal muscle , 2013 .

[55]  D. Allen,et al.  Impaired calcium release during fatigue. , 2008, Journal of applied physiology.

[56]  D. Allen,et al.  Skeletal muscle fatigue: cellular mechanisms. , 2008, Physiological reviews.

[57]  M. Hoth,et al.  Potent Inhibition of Ca 2 Release-activated Ca 2 Channels and T-lymphocyte Activation by the Pyrazole Derivative BTP 2 * , 2004 .

[58]  A. Dulhunty,et al.  Calsequestrin is an inhibitor of skeletal muscle ryanodine receptor calcium release channels. , 2002, Biophysical journal.