The Bcl-2 family of proteins is crucial for apoptosis (a form of programmed cell death) regulation. They target the mitochondrial outer membrane where they interact to determine cell fate. We will evaluate the membrane interactions of the Bcl-2 proteins in complementary biophysical and cellular experiments to redefine our understanding of the mechanism of apoptosis and provide new avenues for the development of compounds to selectively modulate diseases in which apoptosis is unregulated.
Myo1b Bridges The Actin-membrane Interface During Osteoclastic Bone Resorption
Funder
National Health and Medical Research Council
Funding Amount
$429,387.00
Summary
Osteoporosis is a debilitating bone disease which features progressive bone loss. Bone loss (resorption) is driven by the bone resident cell the osteoclast. Identifying molecules that regulate bone resorption by osteoclasts is a crucial first step towards developing new targets for theraputic intervention. This proposal explores the role of Myo1b, a novel protein that appears to facilitate osteoclastic bone resorption and thus represents an attractive new candidate to target bone loss.
Mechanism Of Bacterial Resistance To Antimicrobial Peptides
Funder
National Health and Medical Research Council
Funding Amount
$675,585.00
Summary
Bacterial resistance to antibiotics continues to emerge and intensify. While antimicrobial peptides (AMPs) are a promising alternative to current antibiotics, bacteria have also evolved resistance mechanisms to them through changes in their cell membrane. This application will apply a range of analytical and biophysical tools to understand how bacteria change their cell walls in response to AMPs. The results will allow us to design new combination therapies to treat bacterial infections.
Epigenetic Regulation Of Inflammatory Genes In The Fetal Membranes: Role In Term And Preterm Birth
Funder
National Health and Medical Research Council
Funding Amount
$468,534.00
Summary
Preterm birth is the leading cause of death among newborns and the biggest contributor to disability among infants. Here we propose research to define the mechanism that controls the length of pregnancy and is disrupted in preterm birth. Specifically, we will determine what causes the repression of the labour-promoting inflammatory genes in the uterus during pregnancy and what activates them at labour. We will identify new targets for interventions to block or prevent preterm birth.
Immunomodulatory Properties Of Amnion: From Pregnancy To Regenerative Medicine
Funder
National Health and Medical Research Council
Funding Amount
$446,349.00
Summary
Cells from the placenta have been shown to have regenerative capabilities, repairing injured tissues. In this research we aim to explore how the cells do this. In particular we will address how transplanted placental cells talk to the recipient's immune cells to better coordinate tissue repair and prevent scarring. In short, we aim to learn how these cells coordinate immune function during pregnancy to then apply this knowledge to regenerative medicine.