I am a biochemist - cell biologist investigating the molecular coordination of cellular processes that regulate metabolism. My research aim is to identify and validate novel therapeutic targets - strategies that will ameliorate the metabolic complications
Pathways Involved In The Insulin-like Growth Factor (IGF)-independent Actions Of IGF Binding Protein-6
Funder
National Health and Medical Research Council
Funding Amount
$550,725.00
Summary
Insulin-like growth factors (IGFs) are important proteins that regulate growth. When not regulated properly, diseases such as cancer can occur. A family of IGF binding proteins regulates IGFs. IGFBPs may inhibit IGFs and we have shown that one of them, IGFBP-6, decreases growth of some experimental cancers. As well as regulating IGFs, some IGFBPs alter cell behaviour independently of IGFs, and we found that IGFBP-6 stimulates cell movement in this way. We will now determine how this happens.
Obesity is associated with type 2 diabetes, fatty liver disease, cardiovascular disease and cancer. These inter-related diseases reduce life expectancy and their treatments come at an enormous financial cost. The overriding aim of this work is to understand the molecular and cellular regulation of lipid metabolism in skeletal muscle, liver and adipose tissue, and how this impacts endocrine function to affect the pathogenesis of types 2 diabetes and prostate cancer.
ROLE OF RIP KINASES & IAPs IN MUCOSAL IMMUNE DEFENCE
Funder
National Health and Medical Research Council
Funding Amount
$631,168.00
Summary
Pathogenic bacteria are master manipulators of the inflammatory signalling pathways designed to thwart them. Understanding how they do this will allow us to develop drugs that limit their ability to infect. We have shown that pathogenic bacteria inject a protein called EspL into human cells to promote the destruction of a family of human proteins, called RIP Kinases (RIPK), that co-ordinate the inflammatory response and aim now to discover how EspL causes RIPK degradation and thereby promotes in ....Pathogenic bacteria are master manipulators of the inflammatory signalling pathways designed to thwart them. Understanding how they do this will allow us to develop drugs that limit their ability to infect. We have shown that pathogenic bacteria inject a protein called EspL into human cells to promote the destruction of a family of human proteins, called RIP Kinases (RIPK), that co-ordinate the inflammatory response and aim now to discover how EspL causes RIPK degradation and thereby promotes infection.Read moreRead less
The Effect Of Α-actinin 3 Deficiency On Regulation Of Skeletal Muscle Mass In Health And Disease.
Funder
National Health and Medical Research Council
Funding Amount
$84,800.00
Summary
A common genetic variant results in absence of the fast muscle fibre protein ?-actinin-3 in more than one billion humans worldwide. Loss of ?-actinin-3 influences elite athletic performance, muscle bulk and strength in the general population, and disease severity in muscle wasting conditions. The goal of this study is to understand how ?-actinin-3 regulates muscle mass so that individuals at increased risk of muscle wasting may be identified and treated accordingly.
Identifying A Novel Role For Pigment Epithelium-derived Factor In Obesity-related Metabolic Dysfunction
Funder
National Health and Medical Research Council
Funding Amount
$361,637.00
Summary
Obesity is an important factor contributing to insulin resistance and type 2 diabetes; however, the factors linking these disorders are not well defined. A protein called PEDF is elevated in obesity and type 2 diabetes. This project will examine how PEDF causes insulin resistance and whether blocking PEDF's actions prevents insulin resistance. Successful completion of this project may lead to therapeutics that reduce the risk of developing type 2 diabetes.
The Effects Of ACTN3 R577X On Muscle Wasting And Repair, And Response To Therapy
Funder
National Health and Medical Research Council
Funding Amount
$1,066,054.00
Summary
Complete loss of ACTN3 is normal and occurs in 1 in 5 people world-wide. While it does not cause disease, loss of ACTN3 results in ~10% reduction in muscle mass and strength. This has tremendous impact not only on the success of elite athletes but also the quality of life in people who are already frail. Precisely how ACTN3 affects muscle mass is unclear. Understanding this will help identify the patients who are at greater risk of muscle wasting and also the therapies that will best treat them.
Interactions Of Gastric Hormones With Vagal Afferent Pathways And The Role Of This System In Obesity
Funder
National Health and Medical Research Council
Funding Amount
$550,918.00
Summary
When we feel full after a meal it is the result of a variety of different nerve signals from the gut in response to distension of the stomach and specific nutrients. These signals are disordered in obesity and this project aims to find out how to correct this problem in this modern day epidemic.