Education and Training
1989 - 1993 BA, Biology, Luther College
1997 - 1999 PhD student, University of Iowa, Molecular Physiology and Biophysics
Thesis Advisor – Brett A. Adams, PhD
1999 - 2003 PhD, Biology (Neurobiology), Utah State University,
Thesis Advisor – Brett A. Adams, PhD
“Muscarinic modulation of neuronal voltage-gated calcium channels.”
Post Graduate Education and Training
2003 - 2005 Postdoc, Colorado State University, Department of Biomedical Sciences,
Mentor – Kurt G. Beam, PhD
2005 - 2008 Postdoc, University of Colorado SOM, Department of Physiology and Biophysics,
Mentor – Kurt G. Beam, PhD
I began my career as a PhD student in the laboratory of Dr. Brett Adams, first at the University of Iowa, then at Utah State University. There, my thesis cenetered on G protein-dependent modulation of voltage-gated calcium channels. After earning my degree, I moved to Colorado State University for two years post-doctoral study with Dr. Kurt Beam in order to study the molecular underpinnings of excitation-contraction coupling in skeletal muscle. I then moved to the Department of Physiology and Biophysics at the University of Colorado School of Medcine for another six years of postdoctoral training with Dr. Beam. In July 2011, I was appointed to Assistant Professor postion in the Department of Medicine at the University of Colorado and promoted to Associate Professor in July 2019. During this time, I established an independent laboratory which largely focused on interactions between L-type calcium channels and RGK family small G proteins. In August 2019, I moved my laboratory to University of Maryland School of Medicine because of its strengths in skeletal muscle and ion channel research.
skeletal muscle, excitation-contraction coupling, ion channels, gating, calcium channel, amyotrophic lateral sclerosis, episodic ataxia type 2
Beqollari D, Romberg CF, Meza U, Papadopoulos S, Bannister RA (2014) Differential effects of RGK proteins on L-type channel function in adult mouse skeletal muscle. Biophys J 106:1950-1957.
Beqollari D, Romberg CF, Filipova D, Meza U, Papadopoulos S, Bannister RA (2015) Rem uncouples excitation-contraction coupling in mouse skeletal muscle fibers. J Gen Physiol 146:97-108.
Beqollari D, Romberg CF, Dobrowolny G, Martini M, Voss AA, Musarò A, Bannister RA (2016) Progressive impairment of CaV1 function in the skeletal muscle of mice expressing a mutant Cu/Zn superoxide dismutase 1 (G93A) linked to amyotrophic lateral sclerosis. Skelet Muscle 6:24.
Beqollari D, Dockstader K, Bannister RA (2018) A skeletal muscle L-type Ca2+ channel with a single mutation in the selectivity filter (CaV1 E1014K) conducts K+. J Biol Chem 293:3126-.-3132..
Tyagi S, Filipova D, Bendrick TR, Papadopoulos S, Bannister RA (2019) A mutation in CaV1 linked to a severe neurodevelopmental disorder impairs channel gating. J Gen Physiol 151:850-859.
Meza U, Bannister R, Melliti K, Adams B (1999) Biphasic, opposing modulation of cloned neuronal a1E Ca2+ channels by distinct signaling pathways coupled to M2 muscarinic acetylcholine receptors. J Neurosci 19:6806-6817.
Zealear DL, Swelstad MR, Sant’Anna GD, Bannister RA, Billante CR, Rodriguez RJ, Garren KC, Billante MJ, Champney MS (2001) Determination of the optimal conditions for laryngeal pacing with the Itrel II implantable stimulator. Otolaryngol Head Neck Surg 125:183-92.
Bannister RA, Melliti K, Adams BA (2002) Reconstituted slow muscarinic inhibition of neuronal L-type (CaV1.2c) Ca2+ channels. Biophys J 83:3256-3267.
Bannister RA, Melliti K, Adams BA (2004) Differential modulation of cloned R-type Ca2+ channels by Gaq/11-coupled muscarinic receptors. Mol Pharmacol 65:381-388.
Papadopoulos S, Leuranguer V, Bannister RA, Beam KG (2004) Mapping sites of potential proximity between the DHPR and RyR1 in muscle using a CFP-YFP tandem as a FRET probe. J Biol Chem 279:44046-44056.
Bannister RA, Beam KG (2005) The a1S N-terminus is not essential for bi-directional coupling with RyR1. Biochem Biophys Res Commun 336:134-141.
Meza U, Thapliyal, Bannister RA, Adams BA (2007) Neurokinin 1 receptors trigger overlapping stimulation and inhibition of CaV2.3 (R-type) calcium channels. Mol Pharmacol 71:284-293.
Bannister RA (2007) Bridging the myoplasmic gap: Recent developments in skeletal muscle excitation-contraction coupling. J Musc Res Cell Motil 28:275-283.
Bannister RA, Colecraft HM, Beam KG (2008) Rem inhibits excitation-contraction coupling in skeletal muscle by down-regulating the number of functional L-type Ca2+ channels. Biophys J 94:2631-2638.
Bannister RA, Grabner M, Beam KG (2008) The a1S III-IV loop influences DHPR gating but is not directly involved in excitation-contraction coupling interactions with the type 1 ryanodine receptor. J Biol Chem 283:23217-23223.
*Thapliyal A, *Bannister RA, Hanks C, Adams BA (2008) The monomeric G proteins AGS1 and Rhes selectively influence Gai-dependent signaling to modulate N-type (CaV2.2) calcium channels. Am J Physiol-Cell Physiol 295:C1417-C1426.
Bannister RA, Pessah IN, Beam KG (2008) The skeletal L-type Ca2+ current is a major contributor to Excitation-Coupled Ca2+ Entry (ECCE). J Gen Physiol 133:79-91.
Bannister RA, Papadopoulos S, Haarmann CS, Beam KG (2009) Effects of inserting fluorescent proteins into the a1S II-III loop: insights into excitation-contraction coupling. J Gen Physiol 134:35-51.
Bannister RA, Ohrtman JD (2009) Reassessing the molecular mechanism of b-adrenergic stimulation of cardiac L-type Ca2+ current. Channels 3:146-148.
Dirksen RT, Bannister RA (2009) The 63rd Annual Symposium of the Society of General Physiologists: “Muscles” instead of squid at Woods Hole. J Gen Physiol 134:453-455.
Bannister RA, Beam KG (2009a) The cardiac dihydropyridine receptor a1C subunit can support excitation-triggered Ca2+ entry in dysgenic and dyspedic myotubes. Channels 3:268-273.
Bannister RA, Beam KG (2009b) Ryanodine modification of RyR1 retrogradely affects L-type Ca2+ channel gating in skeletal muscle. J Musc Res Cell Motil 30:217-223.
Estève E, Eltit JM, Bannister RA, Liu K, Pessah IN, Beam KG, Allen PD, López JR (2010) A malignant hyperthermia-inducing mutation in RYR1 (R163C): alterations in Ca2+ entry, release and retrograde signaling to the DHPR. J Gen Physiol 135:619-628.
Bannister RA, Estève E, Eltit JM, Allen PD, Pessah IN, López JR, Beam KG (2010) A malignant hyperthermia-inducing mutation in RYR1 (R163C): consequent alterations in the functional properties of DHPR channels. J Gen Physiol 135:629-640.
Beam KG, Bannister RA (2010) Looking for answers to EC coupling’s persistent questions. J Gen Physiol 136:7-12.
Bannister RA, Polster A (2011) A shortcut to a skeletal muscle DHPR knock-in? J Physiol 589:4645-4646.
Bannister RA, Beam KG (2011) Properties of Na+ currents conducted by a skeletal muscle L-type Ca2+ channel pore mutant (SkEIIIK). Channels 5:1-7.
*Cherednichenko G, *Zhang R, *Bannister RA, Timofeyev V, Li N, Fritsch EB, Feng W, Barrientos GC, Schebb NH, Hammock BD, Beam KG, Chiamvimonvat N, Pessah IN (2012) Triclosan impairs excitation-contraction coupling and Ca2+ dynamics in striated muscle. Proc Natl Acad Sci USA 109:14158-14163.
*Eltit JM, *Bannister RA, Moua O, Altamirano F, Hopkins PM, Pessah IN, Molinski TF, López JR, Beam KG, Allen PD (2012) Malignant hyperthermia arising from altered resting coupling between the skeletal muscle L-type Ca2+ channel and the type 1 ryanodine receptor. Proc Natl Acad Sci USA 109:7923-7928.
Bannister RA (2013) Dantrolene-induced inhibition of skeletal L-type Ca2+ current requires RyR1 expression. Biomed Res Int 2013:390493.
Bannister RA, Beam KG (2013) CaV1.1: the atypical prototypical voltage-gated Ca2+ channel. Biochim Biophys Acta-Biomembranes 1828:1587-1597.
Bannister RA, Beam KG (2013) Impaired gating of a mutant CaV1.1 (R174W) linked to malignant hyperthermia susceptibility. Biophys J 104:1917-1922.
Meza U, Beqollari D, Romberg CF, Papadopoulos S, Bannister RA (2013) Potent inhibition of L-type Ca2+ currents by a Rad variant linked to human cardiac hypertrophy. Biochem Biophys Res Commun 439:270-274.
Larson ED, Sumner WA, St. Clair JR, *Bannister RA, *Proenza CA (2013) Depressed pacemaker activity of sinoatrial node myocytes contributes to the age-dependent decline in maximum heart rate. Proc Natl Acad Sci USA 110:18011-18016.
Romberg CF, Beqollari D, Meza U, Bannister RA (2014) RGK proteins inhibit depolarization-dependent Ca2+ entry in developing myotubes. Channels 8:243-248.
Ohrtman JD, Romberg CF, Moua O, Bannister RA, Levinson SR, Beam KG (2015) Apparent lack of physical or functional interaction between CaV1.1 and its distal C-terminus. J Gen Physiol 145:303-314.
Beqollari D, Romberg CF, Filipova D, Papadopoulos S, Bannister RA (2015) Functional assessment of Rem residues identified as critical for interactions with CaVb subunits. Pflügers Archiv-Eur J Physiol 467:2299-2306.
Bannister RA (2015) Bridging the myoplasmic gap II: more recent advances in EC coupling. J Exp Biol 219:175-182
Bannister RA, Sheridan DC, Beam KG (2015) Distinct components of retrograde excitation-contraction coupling revealed by a lethal mutation in the type 1 ryanodine receptor (RyR1 E4242G). Biophys J 110: 912-921.
Beqollari D, Bannister RA (2016) Defining the MOs of RGK proteins. Channels 10:1-3.
Tyagi S, Beqollari D, Lee CS, Walker LA, Bannister RA (2017) Semi-automated analysis of mouse hindlimb muscle fiber-type composition. J Vis Exp http://www.jove.com/video/56024
Meza U, Beqollari D, Bannister RA (2017) Molecular mechanisms and physiological relevance of RGK proteins in the heart. Acta Physiologica 222:e13016.
Beqollari D, Kohrt WM, Bannister RA (2019) Equivalent L-type channel (CaV1.1) function in adult female and male mouse muscle fibers Biochem Biophys Res Commun, in press.
Tyagi S, Ribera AB, Bannister RA (2020) Zebrafish as model system for the study of CaV2.1 (a1A) channelopathies. Front Mol Neurosci 12:329.
We currently have two major projects in the laboratory: 1) understanding how altered plasma membrane excitability contributes to muscle atrophy and the loss of motor units in aging and neuromuscular disease (e.g., amyotrophic lateral sclerosis; ALS), and 2) using heterologous systems and zebrafish models to study CACNA1A mutations that result in molecular, synaptic and behavioral defects and to screen for effective drug therapies to combat these and other CaV2.1 channelopathies.
2011 Traveling Scholar Award w/ C.A. Proenza, Society of General Physiologists
2014 Webb-Waring Investigator, Boettcher Foundation
2014 Butler-Williams Scholar, NIH/NIA
2015-present Member, Faculty of 1000 Neuroscience Faculty
2019 Oustanding MS thesis, CU-Boulder Graduate School (S.Tyagi, student; R.A. Bannister, mentor)
1999-present General Member, The Biophysical Society, Membrane Biophysics subgroup
2005-2007 General Member, Society for Neuroscience
2007-present General Member, Society of General Physiologists
2008-2010 Councilor, Society of General Physiologists
2009-2011 General Member, The Physiological Society
2012-2014 General Member, American Heart Association
2018-present General Member, Society for Neuroscience
2019-present General Member, National Ataxia Foundation
NIH, NINDS, R01-NS103777, “Rad and amyotrophic lateral sclerosis (ALS)”
NIH, NIA, R03-AG065626, "Impact of Rad-mediated inhibition of CaV1.1 on skeletal muscle composition and contractility”
National Ataxia Foundation, Seed Grant, "Zebrafish as a model system for the study of severe CaV2.1 channelopathies"
Electrophysiology, calcium imaging, zebrafish, heterologous systems