Principal speaker
Professor Katsuhiko Muraki
Understanding Chronic Conditions Topic 14: Neuroimmunology and Emerging Diseases
Biography
Prof Katsuhiko Muraki – is Professor of Cellular Pharmacology, School of Pharmacy at Aichi-Gakuin University, Nagoya Japan and Visiting Professor of Multidisciplinary Cardiovascular Research Centre at University of Leeds, Leeds UK. He received his PhD degree in 1990 from Nagoya City University. From 1989 to 1991, he was a young research fellow of Japan Society for the Promotion of Science and carried out postdoctoral research at Department of Pharmacology and Clinical Pharmacology of St. George's Hospital Medical School in UK. Until 2005, he was a research scientist of smooth muscle electrophysiology in Department of Chemical Pharmacology directed by Professors Yuji Imaizumi and Minoru Watanabe at Nagoya City University.
Katsuhiko Muraki's recent research interests have focused around ion channel pharmacology, particularly drugs on transient receptor potential (TRP) channel. He has had international collaborations with Professor David Beech's group in UK, Professor Eeva Moilanen's group in Finland, and Professor Sonya Marshall-Gradisnik and Professor Don Staines group in Australia.
Abstract
Prof Katsuhiko Muraki – (-)Englerin A: Is it a miracle natural compound for TRPC1/C4/C5 channels?
A sesquiterpene, (-)Englerin A (EA), which is an organic extract of the plant Phyllanthus engleri Pax, has been reported to be an effective inhibitor of renal cancer cell growth. The potent activity of EA is currently explained by two distinct targets, nPKCθ, a member of the novel protein kinase C isoform (nPKC) and TRPC1/C4/C5 channels, members of transient receptor potential canonical subfamily (TRPC). It is also demonstrated that ceramides may be a mediator of some actions of EA.
Which targets have a strong connection to cancer pathology? In this presentation, our recent data are summarized and it is proposed that heteromeric TRPC1/C4 channel is a primary target of EA, with biophysical, pharmacological and molecular biological approaches. Moreover, our recent studies have revealed that Na+ loading into cancer cells is toxic via EA-induced activation of the heteromeric TRPC1/C4 channel and a pretreatment with Pico145, a novel synthetic inhibitor of TRPC1/C4/C5 channels, restores the cell viability. However, several reports on EA still include some conflicts and hence further extensive works will be required for the way forward to the clinic.
Please RSVP here. This is for catering purposes and for MenziesHIQ to stay in touch with you to advise of any potential changes, should they occur
Event categories
RSVP
RSVP on or before Tuesday 29 August 2017 , by email uccmenzieshiq@griffith.edu.au , or by phone 07 56780907