Directvote Election: Candidate Bios

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Directvote Election: Candidate Bios DirectVote Election: Candidate Bios President-Elect Your Voting Status: Select 0 to 1 from below. Selected: 0 Vote For: Diane Lipscombe Diane Lipscombe Administrative Accomplishments: Throughout my career, I have had numerous opportunities, with increasing complexity and scope, to combine my strong commitment to neuroscience research with my administrative leadership skills in the service of my department and at the level of the university, as well as through professional societies and non-profit organizations. I gain tremendous personal gratification from organizational problem-solving efforts that require creating new programs and improving existing ones, toward enhancing research and training in neuroscience and its communication to scientific and lay audience. I have learned the importance of community-wide engagement, effective communication, and building consensus around major issues. A key ingredient to reaching fair decisions and establishing enduring programs is seeking broad input at all levels, including from students and postdoctoral trainees, and engaging a diversity of opinions to reflect the broad community of researchers. At Brown, I have served in a number of roles that require combined administrative and scientific skills. I directed the graduate program in neuroscience for six years and since 2006, I have been the Principal Investigator on Institutional Training Grants that have supported graduate education and diversity in the Neuroscience Graduate Program at Brown. Under my leadership, the program began its successful relationship with the NIH Graduate Partnership Program. Currently, I am the Director of the Brown Institute for Brain Science, a multidisciplinary institute that engages more than 100 research laboratories in over 10 departments in both the basic and clinical sciences. I was appointed director in 2016, having served as interim director during the 18 months prior. The main purpose of the Institute is to promote integrative research in neuroscience and brain science across the university community. At Brown University, I have also contributed to university- wide governance as Vice Chair of the Academic Priorities Committee and Chair of the Tenure Promotions and Appointments Committee, in addition to a range of other committee memberships. My service has extended beyond Brown within my local community; I currently serve on the Board of Directors of the Care New England Health Care System in Rhode Island, and I was previously on the board of the Butler Psychiatric Hospital in Providence, RI. I have served on a number of national committees; I serve on SfN council, was Chair of the Scientific Publications Committee for SfN and the working group that ultimately led to eNeuro; I was recently approved for appointment to the Board of Scientific Counselors for NINDS; and I am an elected fellow and member of the Neuroscience steering group for the American Association for the Advancement of Science (AAAS). https://www.directvote.net/sfn/app/bio_page.aspx?item=1&option=1001&return=ballot_page.aspx[5/11/2017 3:05:34 PM] DirectVote Election: Candidate Bios Degree, Institute, Year Earned: BSc, University College London, 1982 PhD, University College London, 1986 Postdoctoral Research Associate, Yale University School of Medicine, 1986-1989 Postdoctoral Research Fellow, Stanford School of Medicine, 1989-1990 Research Areas: My laboratory’s research focuses on the role of ion channels, particularly voltage-gated calcium ion channels, in neuronal function in normal and disease states. We investigate properties of ion channels including their modulation, regulation by cell-specific alternative splicing, role in nociceptors to mediate acute and chronic pain signaling, and potential importance in the pathophysiology of disorders. Through collaborations, we also seek to define defects in early stage animal models of ALS and are developing new molecular tools to regulate neuronal activity. Current Position(s) at Your Current Institution: Director, Brown Institute for Brain Science Professor of Neuroscience, Department of Neuroscience Memberships: Society for Neuroscience Councilor, 2015-2019 Member, Ethics Committee, 2013-2014 Chair, Scientific Publications Committee, 2011-2014 Member, Scientific Publications Committee, 2008-2011 American Association for the Advancement of Science (AAAS) Member-at-large for Neuroscience, 2015-2018 Elected Fellow, 2013 Society of General Physiologists Council, 2001-2004 Service Positions: A. Editorial Boards: Current Opinions in Physiology Editorial Board, 2017-present Channels Editorial Board, 2012-present Journal of Neurophysiology Editorial Board, 2012-2015 Brain Research Senior Editor, 2011-2013 Wiley Interdisciplinary Reviews Editorial Board, 2010-2014 Journal of Neuroscience Editorial Board/Reviewing Editor, 2003-2007 B. Other Service Positions: NIH/NINDS Approved to serve on Board of Scientific Councilors, 2017-2021 NIH, Office of the Director External advisory board, NIH Director’s Biomedical Research Workforce Innovation Award Broadening Experiences in Scientific Training (BEST), 2014-2018 NIH CSR Chair, BPNS Study Section, 2015-2016 https://www.directvote.net/sfn/app/bio_page.aspx?item=1&option=1001&return=ballot_page.aspx[5/11/2017 3:05:34 PM] DirectVote Election: Candidate Bios Member, BPNS Study Section, 2010-2016 Care New England, Health Care System (Providence, RI) Board of Directors, 2012-present Member, Academic Council, 2012-present Marine Biological Laboratories (Woods Hole, MA) Fellow Selection Committee, 2001-2004 NIH, CSR Member, MDCN3 Study Section, 1999-2003 Marine Biological Laboratories Summer Neurobiology Course Instructor, 1993-1998 Science Biography: My scientific career started when, by a stroke of good fortune, I joined James W. Black’s laboratory as a technician at Burroughs Wellcome in the UK. He was instrumental in my joining the Pharmacology Department at University College London in 1979. I was in awe of the ability to record electrical signals in real time from neurons, even down to the resolution of single molecules. I found the study of neuroscience dynamic and exciting, and an intellectual nucleus of disciplines from across the biological and physical sciences. Joining Richard W. Tsien’s lab in 1986 was the beginning of my 30- year journey studying neuronal voltage-gated calcium ion (CaV) channels; a road enriched by many talented postdocs, students, and collaborators. Strategically located at every critical step of information transfer in the nervous system, CaV channels have defining roles in a wide variety of functions, from signal detection to perception, from neuronal development to programmed apoptosis, and in memory formation and retrieval. My laboratory has contributed to basic understanding of the molecular and functional diversity of CaV channels, reflecting the functional specialization needed to support a range of specific cellular tasks. I have shared our ion channel clones widely, believing in open access to research reagents, and they are now used by hundreds of labs across the world. Our studies of CaV channels provide gateways to addressing key questions in neuronal signaling in healthy and diseased states. We apply genetic, molecular, electrophysiological, optogenetic, and behavioral approaches to show how tissue-specific RNA splicing regulates the functions of CaV channels. By studying their tissue-specific splicing, we have contributed to knowledge of how this mechanism, prevalent in the nervous system, supports biological complexity. In nociceptors, inhibition of CaV channels by opioid receptors is enhanced by a cell-specific, exon-specified amino acid sequence in the CaV channel. We showed this mechanism has direct relevance to pain processing in normal and chronic pain states, and in doing so identified potential therapeutic targets. We are now defining the cell-specific splicing factors and epigenetic modifiers that control exon choice in specific neuron classes. Through collaborations, we have contributed to biophysical studies of rare schizophrenia risk variants in human CaV channel genes, are developing calcium-sensitive bioluminescent proteins to regulate neuronal activity, and are identifying defects in early-stage disease progression in Drosophila and in mouse models of familial Amyotrophic Lateral Sclerosis. The pace of discovery and progress across the breadth of neuroscience is thrilling. Advances in research already benefit many aspects of human society, inform rational decision-making, assist in device development to restore brain function, and lead to novel interventions to diagnose, prevent, or treat injury and diseases. But much remains to be discovered and critical needs are still unmet. Communicating the value of basic research and the future potential of research to others, beyond our scientific community, is both rewarding and important. As funding support for research and training are under threat, and all too often inadequate, our commitment to sustained local, national, and global advocacy is needed now, more than ever. Curriculum vitae (pdf opens in a new window) 1 https://www.directvote.net/sfn/app/bio_page.aspx?item=1&option=1001&return=ballot_page.aspx[5/11/2017 3:05:34 PM] DirectVote Election: Candidate Bios https://www.directvote.net/sfn/app/bio_page.aspx?item=1&option=1001&return=ballot_page.aspx[5/11/2017 3:05:34 PM].
Recommended publications
  • CURRICULUM VITAE December, 2018 DIANE LIPSCOMBE, Phd
    CURRICULUM VITAE December, 2018 DIANE LIPSCOMBE, PhD Brown University Brown Institute for Brain Science 2 Stimson Avenue Providence, RI 02912 [email protected] EDUCATION 1982 B.Sc. (Hons) 1982: University College London, Department of Pharmacology. 1986 Ph.D. University College London, Department of Pharmacology. Thesis title: “Pharmacology of nicotinic receptors on frog neurones: Electrophysiological studies on intact and dissociated ganglia”. APPOINTMENTS 1978-1982 Technician, the Welcome Research Laboratories, Beckenham, Kent, England. Supervised by Sir James W. Black. Full-time:1978 -1979; summers: 1980-1982. 1982-1986 Graduate Student at University College London, Department of Pharmacology. Supervised by Humphrey P. Rang (FRS) and David Colquhoun (FRS). 1986-1988 Postdoctoral Associate at Yale University School of Medicine, Department of Cellular and Molecular Physiology in the laboratory of Richard W. Tsien. 1989-1990 Postdoctoral Fellow at Stanford Medical School, Department of Molecular and Cellular Physiology in the laboratory of Richard W. Tsien. 1990-1992 Visiting Assistant Professor and consultant, Miles Pharmaceuticals, West Haven, CT. 1990-1993 Assistant Professor of Physiology (Research), Brown University, Division of Biology and Medicine. 1993-1999 Assistant Professor of Neuroscience (Tenure Track), Brown University, Division of Biology and Medicine. 1997 Visiting Assistant Professor in the Centers for Genome Research and for Neuroscience, Edinburgh University, UK. 1999 Associate Professor of Neuroscience (with tenure), Brown University. 2006 Professor of Neuroscience, Brown University. 2014-2015 Co-Director, Center for Neurobiology of Cells and Circuits, Brown Institute for Brain Science. 2015-2016 Interim Director, Brown Institute for Brain Science. 2016 Adjunct Professor of George and Anne Ryan Institute for Neuroscience, University of Rhode Island.
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    RESEARCH ARTICLE Cell-specific exon methylation and CTCF binding in neurons regulate calcium ion channel splicing and function Eduardo Javier Lo´ pez Soto, Diane Lipscombe* The Robert J and Nancy D Carney Institute for Brain Science & Department of Neuroscience, Brown University, Providence, United States Abstract Cell-specific alternative splicing modulates myriad cell functions and is disrupted in disease. The mechanisms governing alternative splicing are known for relatively few genes and typically focus on RNA splicing factors. In sensory neurons, cell-specific alternative splicing of the Cacna1b presynaptic CaV channel gene modulates opioid sensitivity. How this splicing is regulated is unknown. We find that cell and exon-specific DNA hypomethylation permits CTCF binding, the master regulator of mammalian chromatin structure, which, in turn, controls splicing in a DRG- derived cell line. In vivo, hypomethylation of an alternative exon specifically in nociceptors, likely permits CTCF binding and expression of CaV2.2 channel isoforms with increased opioid sensitivity in mice. Following nerve injury, exon methylation is increased, and splicing is disrupted. Our studies define the molecular mechanisms of cell-specific alternative splicing of a functionally validated exon in normal and disease states – and reveal a potential target for the treatment of chronic pain. Introduction The precise exon composition of expressed genes defines fundamental features of neuronal function (Fiszbein and Kornblihtt, 2017; Lopez Soto et al., 2019; Ule and Blencowe, 2019). It is essential *For correspondence: [email protected] to understand the mechanisms that regulate alternative pre mRNA splicing. This dynamic process regulates exon composition for >95% of multi-exon genes according to cell-type and influenced by Competing interests: The development, cellular activity and disease (Furlanis and Scheiffele, 2018).
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