A5031466671- Trace Elements in Health
- Iron Metabolism and Disorders
- Virus-based gene therapy research
- Cell death mechanisms and regulation
- RNA regulation and disease
- Insurance and Financial Risk Management
- Healthcare Policy and Management
- Healthcare Systems and Reforms
- Rabies epidemiology and control
- Autophagy in Disease and Therapy
- Viral Infections and Vectors
- Viral Infections and Outbreaks Research
- Advanced biosensing and bioanalysis techniques
- Technology Adoption and User Behaviour
- Protein Degradation and Inhibitors
- Global Maternal and Child Health
- Financial Literacy, Pension, Retirement Analysis
- FinTech, Crowdfunding, Digital Finance
- ATP Synthase and ATPases Research
- Venomous Animal Envenomation and Studies
- CRISPR and Genetic Engineering
- RNA Interference and Gene Delivery
- Virology and Viral Diseases
- Liver physiology and pathology
- HIV Research and Treatment
Monash University
2009-2024
Australian Regenerative Medicine Institute
2020-2024
The University of Melbourne
2009-2016
Royal Children's Hospital
2009
Murdoch Children's Research Institute
2009
Abstract During apoptosis mediated by the intrinsic pathway, BAX/BAK triggers mitochondrial permeabilization and release of cytochrome- c , followed a dramatic remodelling network that results in herniation subsequent pro-inflammatory components. Here, we show exposure inner membrane (IMM) to cytoplasm, initiates unique form mitophagy deliver these damaged organelles lysosomes. IMM-induced occurs independently canonical PINK1/Parkin signalling is driven ubiquitination IMM. Our data suggest...
The fixed rabies virus (RV) strain Nishigahara kills adult mice after intracerebral inoculation, whereas the chicken embryo fibroblast cell-adapted Ni-CE causes nonlethal infection in mice. We previously reported that chimeric CE(NiP) strain, which has phosphoprotein (P protein) gene from genetic background of lethal mice, indicating P is responsible for different pathogenicities and strains. Previous studies demonstrated RV protein binds to interferon (IFN)-activated transcription factor...
Conventional nuclear import is independent of the cytoskeleton, but recent data have shown that specific proteins can be either facilitated or inhibited by microtubules (MTs). Nuclear P-protein from rabies virus involves a MT-facilitated mechanism, here, we show unique in it also undergoes MT-inhibited import, with mode MT-interaction being regulated oligomeric state P-protein. This first demonstration protein utilise both and mechanisms, switch between these different modes MT interaction...
Granzyme A (GzmA) is secreted by cytotoxic lymphocytes and has traditionally been viewed as a mediator of cell death, although growing body data suggests its physiological role if promotion inflammation. Herein we show that GzmA significantly elevated in the serum chikungunya virus (CHIKV) patients levels correlated with viral load disease scores. CHIKV mouse models showed circulating largely derived from NK cells, no evidence for expression CD4 T cells. Infection mice deficient type I...
Cancer cell metabolism is increasingly recognized as providing an exciting therapeutic opportunity. However, a drug that directly couples targeting of metabolic dependency with the induction death in cancer cells has largely remained elusive. Here we report drug-like small-molecule ironomycin reduces mitochondrial iron load, resulting potent disruption metabolism. Ironomycin promotes recruitment and activation BAX/BAK, but outer membrane permeabilization (MOMP) does not lead to apoptotic...
Granzyme K (GzmK) is a tryptic member of the granzyme family chymotrypsin-like serine proteases produced by cells immune system. Previous studies have indicated that GzmK activates protease-activated receptor 1 (PAR1) enhancing activation monocytes and wound healing in endothelial cells. Here, we show using peptides full length proteins and, to lesser extent related protease GzmA, are capable activating PAR1 PAR2. These cleavage events occur at canonical arginine P1 residue involve exosite...
Rabies virus P-protein is expressed as five isoforms (P1-P5) which undergo nucleocytoplasmic trafficking important to roles in immune evasion. Although nuclear import of P3 known be mediated by an importin (IMP)-recognised localization sequence the N-terminal region (N-NLS), mechanisms underlying other P N-NLS inactive or has been deleted have remained unresolved. Based on previous observation that mutation basic residues K214/R260 C-terminal domain (P-CTD) can result exclusion P3, we used...
Abstract We have recently demonstrated that fibroblast growth factor (FGF)-2 promotes neuroblastoma cell differentiation and overrides their mitogenic response to IGF-I. However, the mechanisms involved are unknown. SK-N-MC cells were cultured with FGF-2 (50 ng/ml) and/or IGF-I (100 up 48 h. Fluorescence-activated sorting analysis indicated G1/G0 cycle phase arrest. Gene expression by RT2-PCR cellular localization showed up-regulation of p21. then investigated whether FGF-2-induced (by GAP43...
MCL-1 is an anti-apoptotic member of the BCL-2 protein family that ensures cell survival by blocking intrinsic apoptotic death pathway 1 . unique in being essential for early embryonic development and many types, including cancer cells, which are not affected loss other members 1–4 Non-apoptotic functions controlling mitochondrial ATP production dynamics have been proposed to underlie this requirement 5–9 The relative contributions versus non-apoptotic normal physiology addressed. Here we...
<div>Abstract<p>Cancer cell metabolism is increasingly recognized as providing an exciting therapeutic opportunity. However, a drug that directly couples targeting of metabolic dependency with the induction death in cancer cells has largely remained elusive. Here we report drug-like small-molecule ironomycin reduces mitochondrial iron load, resulting potent disruption metabolism. Ironomycin promotes recruitment and activation BAX/BAK, but outer membrane permeabilization (MOMP)...
Supplementary Figure from Pharmacologic Reduction of Mitochondrial Iron Triggers a Noncanonical BAX/BAK-Dependent Cell Death
Supplementary Figure from Pharmacologic Reduction of Mitochondrial Iron Triggers a Noncanonical BAX/BAK-Dependent Cell Death
Supplementary Figure from Pharmacologic Reduction of Mitochondrial Iron Triggers a Noncanonical BAX/BAK-Dependent Cell Death
Supplementary Figure from Pharmacologic Reduction of Mitochondrial Iron Triggers a Noncanonical BAX/BAK-Dependent Cell Death
Supplementary Figure from Pharmacologic Reduction of Mitochondrial Iron Triggers a Noncanonical BAX/BAK-Dependent Cell Death