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Brett Simms

Brett Simms Postdoctoral Fellow    
MSc Biomedical Technology, University of Calgary, 2003
PhD Neuroscience, University of Calgary, 2009-14
PhD Dissertation: N-terminal Regulation of L-type Channel Expression and Trafficking

Hotchkiss Brain Institute
Health Research Innovation Center (HRIC) 1B42A
University of Calgary
Calgary Alberta Canada
T2N 4N1
Phone: 403-220-8451
FAX: 403-210-7446
bsimms@hotmail.com

Training / Experience
2002-2003
MSc Biomedical Technology
University of Calgary
Canada

2009 - 2014
PhD Neuroscience
University of Calgary
Canada
Supervisor: Gerald W. Zamponi
Teaching
2010 - 2014
Neur 401 - Advanced Neuroscience Laboratory
KNES 323 - Integrative Human Physiology
CAREERS Health Science Internship
MDSC 619.01 Cellular & Molecular Neuroscience

2014 - 2015
Business Analyst - CEDA
Calgary AB
Canada

2016 -
Postdoctorate
University of Calgary
Calgary Alberta
Supervisor: Dr. R.W. Turner

Awards
PhD
AHFMR Doctoral Studentship, 2010
Cooper Award, MDSC 619.01, 2010


Courses / Certifications
2016 - Workshop - Computational Neuroscience, Univ. Lethbridge, June 2016
2015 - Data Science Specialization - John Hopkin's Coursera
        - SQL Courses 1 & 2
2014 - Mitacs Skills of Communication, University of Calgary
        - Mitacs Project Management I & II
        - Data insights with Power BI in Excel 2013
2013 - University Teaching Certificate - Taylor Institute for Teaching & Learning, University of Calgary
       



Research Focus: Cav3 channel regulation and plasticity cerebellum
Approach: Electrophysiology in vitro, molecular biology, pharmacology
Preparations: Expression systems, in vitro slice preparations
Below are short summaries of my publications.

PhD Thesis research:
My dissertation centered on the regulation of calcium channel expression and trafficking

Postdoctoral research:
My work is focused on the regulation of Cav3 T-type calcium channels and their role in mediating synaptic plasticity

Peer-Reviewed Publications

Simms B.A, Souza I.A., Rehak R., Zamponi G.W. (2014) The amino terminus of high voltage activated calcium channels: CaM you or can’t you. Channels. [Epub ahead of print] http://www.ncbi.nlm.nih.gov/pubmed/24875328

Simms B.A., Souza I.A., Rehak R., Zamponi G.W. (2014) The Cav1.2 N-terminus contains a CaM Kinase site that modulates channel trafficking and function, Pflugers Arch .[Epub ahead of print]
http://www.ncbi.nlm.nih.gov/pubmed/24862738

Simms B.A., Souza I.A., Zamponi G.W. (2014) Effect of the Brugada syndrome mutation A39V on calmodulin regulation of Cav1.2 channels. Molecular Brain 7 (34).

Simms B.A., Zamponi G.W. (2014) Neuronal voltage gated calcium channels: structure, function and dysfunction. Neuron 82 (1): 24-45.

Simms B.A., Souza I.A., Zamponi G.W. (2013) A novel calmodulin site in the Cav1.2 N-terminus regulates calcium-dependent inactivation. Pflugers Arch. [Epub ahead of print] http://www.ncbi.nlm.nih.gov/pubmed/24352630

Simms B.A., Zamponi G.W. (2012) The Brugada syndrome mutation A39V does not affect surface expression of neuronal rat Cav1.2 channels. Molecular Brain 5 (1): 9.

Simms B.A., Zamponi G.W. (2012) Trafficking and stability of voltage-gated calcium channels, Cell Molecular Life Science 69 (6): 843-856.

Altier C., Garcia-Caballero A., Simms B.A., You H., Chen L., Walcher J., Tedford H.W., Hermosilla T., Zamponi G.W. (2011) The CavBeta subunit prevents RFP2-mediated ubiquitination and proteasomal degradation of L-type channels. Nature Neuroscience 14 (2): 173-180.

McRory J.E., Rehak R., Simms B.A., Doering C.J., Chen L., Hermosilla T., Duke C., Dyck R., Zamponi G.W. (2008) Syntaxin 1A is required for normal in utero development. Biochem. Biophys. Res. Commun. 375 (3): 372-377.

Doering C.J., Hamid J., Simms B.A., McRory J.E., Zamponi G.W. (2005) Cav1.4 encodes a calcium channel with low open probability and unitary conductance. Biophys J. 89 (5): 3042-3048.

Doering C.J., Kisilevsky A.E., Feng Z.P., Arnot M.I., Peloquin J., Hamid J., Barr W., Nirdosh A., Simms B.A., Winkfein R.J., Zamponi G.W. (2004) A single Gbeta subunit locus controls cross-talk between protein kinase C and G protein regulation of N-type calcium channels. J Biol Chem. 279 (28): 29709-29717.

Khosravani H., Altier C., Simms B.A., Hamming K.S., Snutch T.P., Mezeyova J., McRory J.E., Zamponi G.W. (2004) Gating effects of mutations in the Cav3.2 T-type calcium channel associated with childhood absence epilepsy. J. Biol. Chem. 279 (11): 9681-9684.

Asmara, H., Ileana M., Rizwan, A.P., Sahu, G., Simms, B.A., Zhang, F-X, Engbers, J.D.T., Stys, P.K., Zamponi, G.W., and Turner, R.W. (2017) A T-type channel-calmodulin complex triggers alpha-CaMKII activation, Molecular Brain, 10:37. PDF.


Book Chapters

Simms B.A. (2014) Brugada syndrome and voltage-gated calcium channels. In: Pathology of Calcium Channels, Weiss N, Koschak A (eds.). 1st ed. New York: Springer Publishing.


Key Abstracts

Asmara, H., Health N.C., Simms B.A., Bartoletti T.M., Rehak R., Micu I., Zhang F.X., Stys P., Zamponi G.W. and Turner R.W. T-type calcium channels form a calcium-dependent complex with calmodulin. Proc. Soc. Neurosci., 2014.

Simms B.A., Assis-Souza I., Black S.A., Zamponi G.W.. A Novel CaMKII interaction in the N-terminus of Cav1.2 Regulates Channel Expression. Fed. European Neurosciences, 2013.

Altier C., Garcia-Caballero A., Simms B.A., Walcher J., Tedford H.W., Hermosilla T., Zamponi G.W. The CavB subunit prevents ubiquitination and proteasomal degradation of L-type calcium channels via the Derlin-1/p97 ERAD protein complex. Biophys. Soc. Abstracts, 2009.

Doering C.J., Hamid J., Simms B.A., Zamponi G.W. and McRory J. Single channel analysis of transiently expressed Cav1.4 voltage-gated calcium channels. Proc. Soc. Neurosci., 2004.

Khosravani H., Altier C., Simms B.A., Federico P., McRory J. and Zamponi G.W. Gating effects of mutations in the Cav3.2 T-type calcium channel associated with childhood absence epilepsy. Canadian Congress of Neurological Sciences, Calgary, Canada, 2004.

Khosravani H., Altier C., Simms B.A., McRory J. and Zamponi G.W. Gating effects of mutations in Cav3.2 associated with childhood absence epilepsy. Biophys. Soc. Abstracts, 2004.

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