Genomes and Genes
Affiliation: University of Rochester
- Ca(2+) permeation and/or binding to CaV1.1 fine-tunes skeletal muscle Ca(2+) signaling to sustain muscle functionChang Seok Lee
Department of Molecular Physiology and Biophysics, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030 USA
Skelet Muscle 5:4. 2015..1 is not required for skeletal muscle excitation-contraction coupling, but whether Ca(2+) permeation through CaV1.1 during sustained muscle activity plays a functional role in mammalian skeletal muscle has not been assessed...
- Monovalent cationic channel activity in the inner membrane of nuclei from skeletal muscle fibersViktor Yarotskyy
Department of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, New York Electronic address
Biophys J 107:2027-36. 2014..Together, these studies characterize a voltage-independent NMCC in skeletal muscle, the properties of which are ideally suited to serve as a countercurrent mechanism during calcium release from the nuclear envelope. ..
- Roscovitine inhibits CaV3.1 (T-type) channels by preferentially affecting closed-state inactivationViktor Yarotskyy
Department of Pharmacology and Physiology, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
J Pharmacol Exp Ther 340:463-72. 2012..The ability of roscovitine to block multiple mediators of proliferation, including CDKs and Ca(V)3.1 channels, may facilitate its anticancer properties...
- Accelerated activation of SOCE current in myotubes from two mouse models of anesthetic- and heat-induced sudden deathViktor Yarotskyy
Department of Physiology and Pharmacology, University of Rochester Medical Center, Rochester, New York, United States of America
PLoS ONE 8:e77633. 2013....
- Temperature and RyR1 regulate the activation rate of store-operated Ca²+ entry current in myotubesViktor Yarotskyy
Department of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, New York, USA
Biophys J 103:202-11. 2012....
- Muscle weakness in myotonic dystrophy associated with misregulated splicing and altered gating of Ca(V)1.1 calcium channelZhen Zhi Tang
Department of Neurology, University of Rochester Medical Center, Rochester, NY 14642, USA
Hum Mol Genet 21:1312-24. 2012..Together, these results indicate that DM-associated splicing defects alter Ca(V)1.1 function, with potential for exacerbation of myopathy...