Keynote Speakers

The team of Dr. Leight A. Swaybe studies the fundamental mechanisms of cellular development in the brain and the heart, in particular, how these processes are controlled by ion channel proteins (large regulated ‘doorways’ enabling ion and metabolite flux across cellular membranes) and their interacting partners. The primary focus of her research centres on pannexin channel proteins, including the role(s) of pannexins in regulating the development of nerve cells as well as the mechanisms that govern pannexin localization within cells. The outcomes of this work have important implications for the understanding of neurodevelopmental disorders, as well as other diseases and disorders involving pannexins within and outside the nervous system. Additionally, part of her team is investigating the role(s) of an ion channel anchoring protein, called ankyrin-B, in heart and nerve cell development in collaboration with Dr. Laura Arbour’s group at the University of British Columbia. Dr. Swayne’s research is currently supported by operating grants from the Canadian Institutes of Health Research and the Natural Sciences and Engineering Research Council of Canada.

Prof. Luc Leybaert has a long standing interest in connexins and calcium signaling. The core research theme of his group is to elucidate mechanisms of intercellular communication and to unravel its intricate linkage to signaling processes in the brain and cardiovascular system. Since his PhD and postdoc time this has always involved a blend of calcium- and connexin-related aspects. His team’s work over the past few years has been directed at understanding the role and regulation of connexin-based intercellular communication and developing peptide tools to interfere with connexin hemichannel function. Work with these tools has demonstrated that Cx43 hemichannels can be considered as novel targets for therapeutic intervention of brain and cardiovascular diseases. Peptides identical to intracellular and extracellular Cx43 domains were found to limit apoptosis spread in glioma cells, to modulate vascular contractility and permeability, to prevent blood-brain barrier leakage, to block fear memory, to mitigate seizure activity, and to protect against cardiac ischemia/reperfusion and cryopreservation-induced injury in human blood vessels, embryos and oocytes. The group is currently engaged in several national and international collaborations aiming to explore connexin channels as molecular targets in animal models of epilepsy, stroke and post-ischemic cardiac arrhythmogenesis, all with translational potential and paving the way towards development of small molecules for use in large animal models. The detailed knowledge on connexin channel regulation and its modulation by peptides has generated significant insights that are crucial for future developments in the field. The group possesses the necessary skills and technology to conduct cardio- and neuro-oriented experimental research lines specifically focusing on connexin remodeling, patch clamp channel studies, calcium imaging studies, and translational animal disease models

Patricia Martin is a Reader in Cell Biology and Principal Investigator within the School of Health and Life Sciences at Glasgow Caledonian University. She was the Bio-Research group lead forthe strategic theme of the Molecular Mechanisms underpinning Long term conditions from2015-2017. In 2017 she hosted IGJC2017 (www.igjc2017.com) in Glasgow attracting over 200 international delegates to the 5 day focussed meeting. She has been a member of the international Gap Junction community since 1994 when she first worked with Professor Howard Evans, University of Cardiff, and was involved in early studies on the efficacy of Connexin mimetic peptides such as Gap27 on regulating channel behaviour. In 2004 she moved to Glasgow establishing the Connexin Research Team within GCU and collaborates closely with industry and clinicians and co-ordinates the GCU Research Skin Tissue Bank. Her specific area of research is the role of connexins in health and disease states including chronic non-healing wounds, psoriasis and other hyperproliferative skin disorders, with a focus on connexins as therapeutic targets. She has supervised over 10 PhD students in this area of research and has secured > £1.5M in research funding and has published widely in the field (>60 publications).
As part of the Bio-GCU-Research-Teaching Team Patricia is the Senior Postgraduate Research tutor responsible for overseeing the progression of over a cohort of over 20 Bio-PhD students. Before joining GCU Patricia held postdoctoral fellows at the University of Wales (1994-2003),
where she established her work on Connexins; University Wageningen, The Netherlands (1992-1993) and the University of Wurzburg, Germany (1991-1992). She has a PhD in Molecular Virology from the University of Warwick and graduated with BSc Hons in Biochemistry with Microbiology from St Andrews University.

Dr. Sorgen lab is committed to advancing our understanding of the fundamental mechanisms of gap junction regulation, with particular interest in protein-protein interactions mediated by the carboxyl terminal (CT) domain of connexins. Over the past two decades, his group has been productive in this area of research, and have been instrumental in the development of new molecular and atomic models to explain the process of gap junction channel assembly, gating, and degradation. They have biophysically characterized and solved the structures of several connexin-related peptides, proteins, and protein/protein complexes that have provided mechanistic insight into the regulation of gap junctions. Their studies thus far have defined a structural change in the cytoplasmic loop of Cx43 that is the likely source of the “receptor” in the “particle-receptor” hypothesis for Cx43 channel closure by intracellular acidification, identified that phosphorylation alters the conformational preference of the Cx43CT, and found that the molecular mechanisms underlying loss of Cx43 from the intercalated disks following myocardial infarction include an interaction of c-Src with ZO-1 and subsequent loss of the scaffolding of Cx43 leaving Cx43 free to diffuse to the lateral myocyte membrane. More recent cell biology and animal studies from his lab have identified and characterized novel tyrosine kinases and phosphatases that influence the interplay between Cx43 and Cx45 gap junction intercellular communication in the normal and diseased state as well as described some of the connexin protein partners affected by Src and MAPK phosphorylation.

Prof. Viviana Berthoud group is interested in understanding the cellular, biochemical and functional behavior of connexins, the gap junction-forming proteins, and in elucidating the mechanism(s) by which connexin abnormalities lead to disease. Her group has focused attention on the mutations in the lens fiber cell connexins which are linked to inherited human cataracts. They have found that most of these mutants do not form functional channels due to a wide gamut of biochemical and cellular alterations including impaired trafficking and altered degradation. This presentation will highlight the variety of alterations caused by these mutants and their convergence on a similar final outcome: impairment of the lens circulation leading to calcium accumulation and cataracts caused by biomineralization.