Recent Graduates - Catterall Lab
Graduate Students Since 2010
PhD in Pharmacology in 2012. Christine studied our mouse model of Dravet Syndrome using a Floxed mouse line in which the Scn1a gene encoding the Nav1.1 brain sodium channel was selectively deleted in forebrain GABAergic interneurons using Cre recombinase driven by the Dlx1,2 intergenic enhancer. She showed that deletion of Nav1.1 channels in forebrain GABAergic interneurons is sufficient to cause the epilepsy, autism, and cognitive deficit of Dravet Syndrome. Her dissertation research was published in first-author papers in Proceedings of the National Academy of Sciences and Channels and in collaborative papers in Nature, Journal of Clinical Investigation and Journal of Pharmacology & Experimental Therapeutics. She is now a postdoctoral fellow with Dr. John Oakley, Assistant Professor of Neurology and Adjunct Assistant Professor of Pharmacology at the University of Washington studying effects of the Dravet Syndrome mutation on the electroencephalogram and local field potentials in hippocampus and cerebral cortex.
PhD in Neurobiology & Behavior in 2012. Karina's thesis research examined the role of calcium sensor proteins as modulators of presynaptic Cav2.1 calcium channels and short-term synaptic plasticity. She established the difficult superior cervical ganglion (SCG) neuronal cell culture system in our laboratory, and she used it to measure synaptic transmission initiated by wild-type and mutant Cav2.1 channels expressed specifically in single presynaptic cells. She found that overexpression of the calcium sensor proteins visinin-like protein 2 and neuronal calcium sensor-1 (NCS-1) increased facilitation of transfected Cav2.1 channels and induced short-term facilitation of synaptic transmission in superior cervical ganglion synapses. In contrast, overexpression of calcium binding protein-1 (CaBP1) increased inactivation of Cav2.1 channels and enhanced a rapid phase of depression of transmission in SCG neuron synapses. Her thesis work was published in a first-author paper in Proceedings of the National Academy of Sciences and a collaborative paper in Molecular & Cellular Neuroscience. She is now a postdoctoral fellow in the laboratory of Professor Henrique von Gersdorff at the Vollum Institute of Oregon Health & Science University, where she is studying regulation of synaptic transmission in the retina.
PhD in Pharmacology in 2012. Jinti's thesis research led to development of a detailed structure-function map of the binding and modulation of voltage-gated sodium channel Nav1.2 by the α-scorpion toxin LqhII, which specifically slows fast inactivation of sodium channels. Her studies showed that the wedge-shaped peptide scorpion toxin inserts into a natural cleft between the S1-S2 and S3-S4 helical hairpins in the voltage-sensing module in domain IV. Binding of the toxin locks the voltage sensor in a partially activated position and prevent coupling of voltage-dependent activation of the channel to fast inactivation. Her thesis research was published in a first-author paper in the Proceedings of the National Academy of Sciences and in a collaborative paper in the Journal of Biological Chemistry in 2011. She joined the biotech industry immediately after graduation, and she is now a Research Scientist in Neuroscience at Amgen in Cambridge MA engaged in drug discovery related to ion channels.
Joel Zongli Zhang
PhD in Molecular & Cellular Biology in 2011. Joel's thesis research led to development of a detailed structure-function map of the binding and modulation of voltage-gated sodium channel Nav1.2 by the β-scorpion toxin CssIV, which specifically impedes voltage-dependent activation of sodium channels. His studies showed that the wedge-shaped peptide scorpion toxin inserts into a natural cleft between the S1-S2 and S3-S4 helical hairpins in the voltage-sensing module in domain II. Binding of the toxin locks the voltage sensor in a fully activated position and thereby greatly enhances voltage-dependent activation of the channel. Joel's thesis research was published in a collaborative paper in the Journal of Biological Chemistry in 2010 and in two first-author papers in the Journal of Biological Chemistry in 2011 and 2012. After a brief period of postdoctoral research with Professor Jeffrey Holt at Harvard Medical School, Joel is now pursuing further training and research in bioinformatics at Massachusetts Institute of Technology.
PhD in Neurobiology & Behavior in 2011. Sung's thesis research gave dramatic new insights into Dravet Syndrome, using our mouse genetic model of that disease. He showed that these mice have a major circadian defect, which is caused by failure of firing of GABAergic interneurons in the suprachiasmatic nucleus (SCN) of the hypothalamus where circadian rhythms originate. He also showed that these mice have autistic-like behaviors, which are caused by failure of firing of GABAergic interneurons in the forebrain and can be ameliorated by treatment with low doses of the benzodiazepine GABA receptor positive allosteric modulator clonazepam. Sung's research from his dissertation and a brief period of postdoctoral research in the lab was published in first-author and co-first author papers in Nature and Proceedings of the National Academy of Sciences in 2012, Neuron in 2014, and Brain in 2015. Sung joined Professor Richard Palmiter's laboratory in the Department of Biochemistry at the University of Washington, where he received a prestigious postdoctoral fellowship from the Life Sciences Foundation. He has been very successful there in studies of the mechanisms of conditioned learning in mice. He is now an Assistant Member of the Salk Institute for Biological Studies and an Adjunct Assistant Professor in Neurobiology at the University of California at San Diego.
PhD in Pharmacology in 2010. Paul's thesis research tested the 'sliding helix' model of voltage-dependent gating using the disulfide-locking method. By substituting cysteine residues for gating charges and their putative ion pair partners, he demonstrated that the gating charges in the S4 segments of the bacterial sodium channel NaChBac make a series of ion pair partners as the S4 segment moves outward during the voltage sensing process. His thesis work was published in a series of four first-author or co-first-author papers in the Proceedings of the National Academy of Sciences in 2008, 2009, 2011, and 2012. Paul went on to a postdoctoral fellowship at the Department of Neurobiology, Harvard Medical School and Boston Children's Hospital, with Professor David Clapham, a leading ion channel researcher. He did pioneering work on ion channels in primary cilia, leading to two back-to-back papers in Nature, and he collaborated in physiological and structural studies of bacterial sodium channels. He was selected for a prestigious K099 New Faculty Development Grant from NIH in 2014, and he began a new position as Assistant Professor of Pharmacology in Northwestern University's Feinberg School of Medicine in 2016.
PhD in Pharmacology in 2016. Teresa studied the molecular mechanisms of ion conductance, selectivity, and drug inhibition of voltage-gated calcium channels using the ancestral bacterial sodium channel NavAb as a molecular template. Bacterial sodium channels like NavAb are evolutionary precursors of mammalian sodium and calcium channels. Together with colleagues in the lab, Teresa made mutations in NavAb to convert it to a calcium-selective form, CavAb, and determined the structures of CavAb and intermediate constructs with calcium bound. These studies revealed a series of calcium binding sites in the pore of CavAb, which bind calcium during ion conductance and release it via a knock-off mechanism when a new calcium ion approaches from the extracellular side. This mechanism explains how the calcium channel can have both high conductance and high selectivity. Teresa went on to study the structural basis for binding of calcium antagonist drugs to CavAb. This work revealed the drug receptor sites for dihydropyridine and phenylalkylamine calcium channel antagonists and elucidated the fundamental structural mechanism for their difference in voltage-dependent and frequency-dependent inhibition, which determines their clinical use in treatment of hypertension and cardiac arrhythmia, respectively. Teresa's work was published in two papers in Nature and in a review article in Molecular Pharmacology.
Postdoctoral Fellows Since 2010Arranged by Date of Departure
Lin Tang, 2017
Professor, State Key Laboratory of Biotherapy, Sichuan University, Cheng Du, China
Joshua Kaplan, 2017
Assistant Professor, Department of Biology, Western Washington University, Bellingham, WA
Evanthia Nanou, 2017
Senior Research Scientist, Vertex Inc., Boston, MA
Haijie Yu, 2016
State Key Laboratory of Quality Research in Chinese Medicines, Macau University of Science & Technology, Macau, China
Jin Yan, 2015
Senior Research Scientist, Molecular Devices, Sunnyvale, CA
Chao Tai, 2015
Senior Research Fellow, Gladstone Institute for Neurological Disease, University of California at San Francisco
Moran Rubinstein, 2015
Assistant Professor, Department of Human Molecular Genetics & Biochemistry, Goldschleger Eye Research Institute, Sackler Faculty of Medicine, Tel Aviv University, Israel
Ying Fu, 2014
Research Scientist, Department of Medicine/Cardiology, Cedars-Sinai Medical Center, University of California at Los Angeles
Franck Kalume, 2012
Venkat Magupalli, 2012
Research Scientist, Boston Children's Hospital and Harvard Medical School
Jian Payandeh, 2012
Senior Research Scientist, Department of Structural Biology, Genentech
John Oakley, 2011
Assistant Professor, Department of Neurology, and Adjunct Assistant Professor, Department of Pharmacology, University of Washington
Vladimir Yarov-Yarovoy, 2011
Associate Professor, Department of Physiology & Membrane Biology, University of California at Davis
Matthew Fuller, 2011
Research Scientist, Drug Discovery, Pfizer, Research Triangle Park, NC
Sylvain Brunet, 2010
Research Associate Professor, Neuroscience, Cleveland Clinic Research Institute, Cleveland, OH
Michelle Emrick, 2010
Research Scientist, Department of Proteomics, VLST Corporation, Seattle