Erick O. Hernandez-Ochoa

Affiliations: 
University of Maryland School of Medicine, Baltimore, MD, United States 
Area:
Autonomous Nervous System, Skeletal muscle, Calcium channels
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"Erick Hernandez-Ochoa"
Mean distance: 15.37 (cluster 11)
 
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Publications

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Melville Z, Hernandez-Ochoa EO, Pratt SJ, et al. (2017) The activation of PKA by the calcium-binding protein S100A1 is independent of cyclic AMP. Biochemistry
Iyer SR, Shah SB, Valencia AP, et al. (2016) Altered nuclear dynamics in MDX myofibers. Journal of Applied Physiology (Bethesda, Md. : 1985). jap.00857.2016
Hernández-Ochoa EO, Pratt SJ, Lovering RM, et al. (2015) Critical Role of Intracellular RyR1 Calcium Release Channels in Skeletal Muscle Function and Disease. Frontiers in Physiology. 6: 420
Hernández-Ochoa EO, Pratt SJ, Garcia-Pelagio KP, et al. (2015) Disruption of action potential and calcium signaling properties in malformed myofibers from dystrophin-deficient mice. Physiological Reports. 3
Hernández-Ochoa EO, Olojo RO, Rebbeck RT, et al. (2014) β1a490-508, a 19-residue peptide from C-terminal tail of Cav1.1 β1a subunit, potentiates voltage-dependent calcium release in adult skeletal muscle fibers. Biophysical Journal. 106: 535-47
Robison P, Hernández-Ochoa EO, Schneider MF. (2014) Atypical behavior of NFATc1 in cultured intercostal myofibers. Skeletal Muscle. 4: 1
Hernández-Ochoa EO, Schachter TN, Schneider MF. (2013) Elevated nuclear Foxo1 suppresses excitability of skeletal muscle fibers. American Journal of Physiology. Cell Physiology. 305: C643-53
Wu F, Mi W, Hernández-Ochoa EO, et al. (2012) A calcium channel mutant mouse model of hypokalemic periodic paralysis. The Journal of Clinical Investigation. 122: 4580-91
Hernández-Ochoa EO, Robison P, Contreras M, et al. (2012) Elevated extracellular glucose and uncontrolled type 1 diabetes enhance NFAT5 signaling and disrupt the transverse tubular network in mouse skeletal muscle. Experimental Biology and Medicine (Maywood, N.J.). 237: 1068-83
Liu Y, Hernández-Ochoa EO, Randall WR, et al. (2012) NOX2-dependent ROS is required for HDAC5 nuclear efflux and contributes to HDAC4 nuclear efflux during intense repetitive activity of fast skeletal muscle fibers. American Journal of Physiology. Cell Physiology. 303: C334-47
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