Signed in as:
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The ACDS is proudly supported by the Pioneers of Australasian cell death research who provide strategic oversight to the society as Honorary Members.
The ACDS Luminaries are valued members who have significantly shaped the field of cell death and continue to lead and inspire the next generation of Australasian scientists.
The societies success is thanks to our motivated and enthusiastic committee of Australasian ECR/MCRs who strive to create a supportive cell death community that values scientific excellence.
The ACDS is committed to fostering equity, diversity, and inclusion in both general scientific practice and the practices of the society.
We recognise that implicit and explicit biases, systemic hurdles, and societal pressures have contributed to under-representation in the scientific pipeline, and that these require an active effort to correct. We aim to maintain equity and diversity in all aspects of our society including our seminar speakers, committee members and ACDS Luminaries by striving for a minimum of 40(F):60(M) gender representation. Our Luminary selection criteria integrates H-index, contribution to the cell death field, and input of ACDS Pioneers. We encourage applications and nominations for ACDS Luminaries from diverse backgrounds.
Prof. Andreas Strasser leads the Blood Cells and Blood Cancer Division at WEHI. He was the first to demonstrate that abnormalities in apoptosis regulation can cause autoimmune disease and cancer, the current focus of his research. Moreover, he identified the two distinct signalling pathways of apoptosis (death receptor or stress signals). Prof. Strasser's contributions have led to the development of BH3 mimetic anti-cancer drugs including venetoclax. He has published over 600 papers which have amassed over 75,000 citations.
Prof. Sharad Kumar leads the Molecular Regulation Lab at the Centre for Cancer Biology, UniSA. He has made many seminal contributions to the cell death field including discovery of caspase-2, Drosophila cell death machineries and a caspase-independent cell death process now known as autophagy-dependent cell death. Prof. Kumar has been awarded the ASBMB Lemberg Medal, FAOBMB Research Excellence Award, ANZSCDB President’s Medal and was appointment as a Member of the Order of Australia.
Prof. Suzanne Cory has devoted a lifetime to understanding the molecular genetics of cancer. With David Vaux and Jerry Adams, they discovered that the oncogene BCL-2, activated by chromosome translocation in human lymphoma, inhibits cells from dying, and synergises with Myc in lymphomagenesis. In addition to her ample research papers that have shaped modern science, Prof. Cory has also shaped the scientific community through her roles as the Director of WEHI (1996-2009) and President of the Australian Academy of Science (2010-2014).
A/Prof. Ruth Kluck is laboratory head at WEHI. She investigates the mitochondrial pathway of apoptosis, focusing on how the BCL-2 protein family regulate mitochondrial permeabilisation. This work began in her PhD and continued into her postdoc where she reported that BCL-2 regulates apoptosis by maintaining mitochondrial integrity. After joining WEHI in 2002, her work has identified key steps in how BAX and BAK change conformation to form pores that commit the cell to die, or become sequestered by pro-survival members.
Prof. Jerry Adams is a laboratory head at WEHI whose research has shaped our understanding of genetics and cell biology. After his initial training with Jim Watson and then Fred Sanger, Jerry’s research has focused on the genetic basis of cancer including discovery of the pro-cancer role of MYC and BCL-2 mutations, and investigates how BCL-2 regulates apoptosis. He has been awarded ample prestigious grants and awards, and frequently publishes in influential journals such as Nature and Science.
Prof. Peter Colman undertook his PhD in physics at the University of Adelaide and transited to structural biology. Postdoctoral work on antibody structure led into studies at CSIRO on the influenza virus antigen neuraminidase and the discovery of zanamivir. In 2001 he moved to WEHI, establishing there the structural biology division which included a team of medicinal chemists. The ensuing collaboration with cell death laboratories at WEHI resulted in industry collaboration and the discovery of venetoclax.
Prof. David Vaux graduated from the University of Melbourne in 1984, then did a PhD at WEHI where he discovered that BCL-2 acted differently to other oncogenes, namely by preventing cell suicide, rather than by promoting cell division. While a post-doc at Stanford, he showed that mammalian apoptotic mechanisms were related to the those in the worm, C. elegans. After returning to Australia in 1993, he and his lab identified the IAP family of proteins in mammals, and their antagonists, including Diablo/Smac and HtrA2.
Dr. Kim Newton is a Principal Scientist in the Physiological Chemistry Department at Genentech (South San Francisco, USA). She obtained her PhD at The University of Melbourne before pursuing a postdoc position at WEHI. Her research explores the relationship between cell death and inflammation, with an emphasis on the signaling mechanisms of FADD, caspase-8, RIPK1, and RIPK3. She is an author of 51 primary publications with 21 of these in Cell, Science or Nature.
Prof. Shigekazu Nagata is currently a laboratory head at iFREC, Osaka University (Japan). After obtaining his Ph.D. as a biochemist at Tokyo University, he was trained as a molecular biologist in Charles Weissmann's laboratory in Zurich and worked with cytokines (human interferon and G-CSF). In the early 1990th, his group in Osaka Bioscience Institute demonstrated that apoptosis could be induced by a death factor (Fas ligand). Since then, he has been asking many fundamental questions about how cells die, how macrophages engulf dead cells, and what happens to the dead cells in macrophages.
Research: Prof Silke's lab seeks to investigate the how, why and when problems of the intersection between cell death and inflammation.
Feature paper: Rickard et al. RIPK1 Regulates RIPK3-MLKL Driven Systemic Inflammation and Emergency Hematopoiesis, Cell, 2014.
Research: The Inflammasome Lab seeks to unravel the secrets of inflammasomes – protein complexes at the heart of inflammation and disease – to allow for new therapies to fight human diseases.
Feature paper: Boucher et al, Caspase-1 self-cleavage is an intrinsic mechanism to
terminate inflammasome activity, Journal of Experimental Medicine, 2018.
Research: The focus of the Fairlie lab is to better understand the mechanisms of apoptosis regulation and to exploit this knowledge for the treatment of disease.
Feature paper: Lee et al, Discovery and molecular characterization of a Bcl-2–regulated cell death pathway in schistosomes, PNAS, 2011.
Research: Focuses on understanding the molecular mechanism underpinning activation of the MLKL pseudokinase by the upstream regulatory kinase, RIPK3, to cause cell death by necroptosis.
Feature Paper: Murphy et al, The pseudokinase MLKL mediates necroptosis via a molecular switch mechanism, Immunity, 2013.
Research: The Hartland Lab studies host-pathogen interactions and the role of cell death in immune defence during bacterial infection.
Feature paper: Pearson et al, EspL is a bacterial cysteine protease effector that cleaves RHIM proteins to block necroptosis and inflammation, Nature Microbiology, 2017.
Research: The Kile lab is focused on understanding mitochondrial-mediated apoptosis, the cellular response to mitochondrial damage, and the link to innate immune signalling.
Feature paper: McArthur et al, BAK/BAX macropores facilitate mitochondrial herniation and mtDNA efflux during apoptosis, Science, 2018.
Research: The Czabotar lab seeks to understand the pathways that govern apoptosis and necroptosis at the molecular level using structural and biochemical techniques, and to use this information to guide drug discovery projects aimed at discovering novel therapeutics for the treatment of diseases characterized by dysregulated cell death.
Feature paper: Czabotar et al, Bax Crystal Structures Reveal How BH3 Domains Activate Bax and Nucleate Its Oligomerization to Induce Apoptosis, Cell, 2013.
Research: The Degli-Esposti lab focuses on understanding the pathways required to improve immune responses to pathogens and malignancies. This involves achieving maximal protection whilst avoiding the “costs” of collateral damage caused by overt inflammation.
Feature paper: Schuster et al, TRAIL+ NK Cells Control CD4+ T Cell Responses during Chronic Viral Infection to Limit Autoimmunity, Immunity, 2014.
Research: The Trapani lab studies the molecular and cellular mechanisms that underpin cytotoxic lymphocyte (CTL/NK)-induced death including determining how CTL/NK cells surveil pre-malignant and malignant cells, harnessing their cytotoxicity as new cancer therapeutics (e.g CAR T cells) and blocking cytotoxicity with inhibitors to prevent auto-immunity and tissue damage.
Feature paper: Voskoboinik et al, Perforin and granzymes: function, dysfunction and human pathology, Nature Reviews Immunology, 2015.
Research: The goal of the Day lab is to discover how the attachment of ubiquitin to proteins is regulated, and how this modification alters protein function. We have focused on understanding the function of ubiquitin ligase proteins that regulate immune and cell survival pathways
Feature paper: Middleton et al, The activity of TRAF RING homo- and heterodimers is regulated by zinc finger 1, Nature Communications, 2017.
Research: Wayne Fairbrother's research has focused on the use of structure-based design methods to identify small-molecule antagonists of apoptotic cell-death regulatory proteins, most notably the inhibitor of apoptosis (IAP) family (GDC-0152 and GDC-0917) and the BCL-2 family (Venclexta), for the treatment of cancer.
Feature paper: Dueber et al, Antagonists induce a conformational change in cIAP1 that promotes autoubiquitination, Science, 2011.
Research: The Huang laboratory is focused on unraveling the control of apoptotic cell death in blood cells and exploiting this knowledge for the development of novel approaches for treating patients with blood cancers.
Feature paper: Chen et al, Differential Targeting of Prosurvival Bcl-2 Proteins by Their BH3-Only Ligands Allows Complementary Apoptotic Function, Molecular Cell, 2005.
Research: The Stacey laboratory is interested in cell death pathways in response to cytosolic DNA, and in the past has characterised AIM2 inflammasome responses and inflammasome recruitment of caspase-8 to initiate apoptosis.
Feature paper: Sagulenko et al, AIM2 and NLRP3 inflammasomes activate both apoptotic and pyroptotic death pathways via ASC, Cell Death and Differentiation, 2013.
Research: The Masters lab aims to learn about the innate immune system from the study of autoinflammatory diseases.
Feature paper: Yu et al, TDP-43 Triggers Mitochondrial DNA Release via mPTP to Activate cGAS/STING in ALS, Cell, 2020.
Research: The Lee lab seeks to understand the mechanisms of apoptosis and autophagy regulation in normal physiology and disease for the development of therapeutics targeting these pathways.
Feature paper: Lee et al, Physiological restraint of Bak by Bcl-xL is essential for cell survival, Genes & Development, 2016.