A5000747636- Autophagy in Disease and Therapy
- Ubiquitin and proteasome pathways
- Mitochondrial Function and Pathology
- PI3K/AKT/mTOR signaling in cancer
- Endoplasmic Reticulum Stress and Disease
- Bone health and treatments
- Bone Metabolism and Diseases
- Erythrocyte Function and Pathophysiology
- Mesenchymal stem cell research
The University of Queensland
2022-2024
South Australian Health and Medical Research Institute
2016-2017
The University of Adelaide
2017
Abstract To maintain both mitochondrial quality and quantity, cells selectively remove damaged or excessive mitochondria through mitophagy, which is a specialised form of autophagy. Mitophagy induced in response to diverse conditions, including hypoxia, cellular differentiation damage. However, the mechanisms that govern removal specific dysfunctional under steady‐state conditions fine‐tune content are not well understood. Here, we report SCF FBXL4 , an SKP1/CUL1/F‐box protein ubiquitin...
The mammalian target of rapamycin complex 1 (mTORC1) is activated by extracellular factors that control bone accrual. However, the direct role this in osteoblast biology remains to be determined. To investigate question, we disrupted mTORC1 function preosteoblasts targeted deletion Raptor (Rptor) Osterix-expressing cells. Deletion Rptor resulted reduced limb length was associated with smaller epiphyseal growth plates postnatal skeleton. caused a marked reduction pre- and accrual, which...
Abstract Since its discovery more than 25 years ago, the STRO-1 antibody has played a fundamental role in defining hierarchical nature of mesenchymal precursor cells (MPC) and their progeny. binding remains hallmark immature pluripotent MPC. Despite significance MPC field, identity antigen remained elusive. Using combination two-dimensional gel electrophoresis, coupled with Western blotting Tandem mass spectroscopy, we have identified as heat shock cognate 70 (HSC70;HSPA8). binds to...
Abstract Mitophagy must be carefully regulated to ensure that cells maintain appropriate numbers of functional mitochondria. The SCF FBXL4 ubiquitin ligase complex suppresses mitophagy by controlling the degradation BNIP3 and NIX receptors, mutations result in mitochondrial disease as a consequence elevated mitophagy. Here, we reveal phosphatase PPTC7 is an essential cofactor for -mediated destruction NIX, suppressing both basal induced Disruption activity not required turnover. Rather, pool...
Abstract Cells selectively remove damaged or excessive mitochondria through mitophagy, a specialized form of autophagy, to maintain mitochondrial quality and quantity. Mitophagy is induced in response diverse conditions, including hypoxia, cellular differentiation, damage. However, the mechanisms by which cells specific dysfunctional under steady-state conditions fine-tune content are not well understood. Here, we report that SCF FBXL4 , an SKP1/CUL1/F-box protein ubiquitin ligase complex,...