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The Role Of Nalp1 In Autoimmune Disease And Innate Immune Defense As Determined By Murine Genetic Deletion.
Funder
National Health and Medical Research Council
Funding Amount
$320,237.00
Summary
The innate immune system is a critical barrier against invading microorganisms, however when improperly regulated it can lead to autoimmune disease. Nalp1 is a protein that is important for innate immune recognition of anthrax infection, and is also involved in susceptibility to vitiligo and associated autoimmune diseases. This project seeks to create mice that are deficient for the gene encoding Nalp1 so as to further study the role of this protein in innate immune defense and autoimmunity.
Effects Of Melanocortin Neurons On Systemic Glucose Homeostasis
Funder
National Health and Medical Research Council
Funding Amount
$860,251.00
Summary
There is good evidence that the brain can control blood glucose, but we do not know how this occurs, or why this doesn’t work in diabetes. This grant will use cutting edge mouse genetic technology to determine how the brain controls blood glucose, and what changes in diabetes. This grant will determine how several hormones act through the brain to change glucose levels, and will help develop new strategies to treat high blood glucose.
Genetic Control Of Body Patterning: Intersection Of Transcriptional And Signalling Activity In Head Formation
Funder
National Health and Medical Research Council
Funding Amount
$579,932.00
Summary
A most critical step in embryonic development is the assembly of the different tissue components into a three-dimensional structure in order to build a major body part of the foetus. The objective of our research is to understand how the mechanisms that control genetic activity and cell-to-cell signalling may cooperate in the formation of the head and face of the embryo. The outcome will focus future clinical investigations to the most relevant genetic determinants of craniofacial defects.
Understanding The Role That Cellular Hypoxia Plays In Normal Heart Development
Funder
National Health and Medical Research Council
Funding Amount
$522,773.00
Summary
Congenital heart defects (CHD) are the most common type of birth defects, being present in 6 out of every 1000 live births, and 10% of stillbirths. In addition to the danger of death during childhood, such heart defects also increase the risk of heart disease during adulthood. Our research project involves looking for the genetic causes of CHD. We are looking at two genes , called HIF1a and CITED2, for which we already have evidence that they are very important in allowing the heart to form norm ....Congenital heart defects (CHD) are the most common type of birth defects, being present in 6 out of every 1000 live births, and 10% of stillbirths. In addition to the danger of death during childhood, such heart defects also increase the risk of heart disease during adulthood. Our research project involves looking for the genetic causes of CHD. We are looking at two genes , called HIF1a and CITED2, for which we already have evidence that they are very important in allowing the heart to form normally within the embryo. Because the heart is the first organ to form in the embryo (during the first trimester), we cannot use humans to study this process. Instead we have two lines of mice which specifically lack either the HIF1a or CITED2 genes throughout the embryo. Both of these mouse lines have severe heart defects similar to some types of CHD seen in humans. However, removal of either of these genes also causes severe defects in other tissues, complicating our study. To overcome this problem, we will use a slightly different technique to remove either gene specifically in the entire developing heart of the embryo, while leaving the normal gene in the rest of the embryo. Thus we will be able for the first time to study the effects of these genes on the heart alone. We suspect that the defects in the hearts of such embryos will be of a particular sub-type of CHD. If this is true, in the future we hope to be able show that mutation of either of these genes will cause a specific type of human CHD. This will enable genetic screening of families with a history of CHD, assist in genetic counselling, and promote the development of therapies.Read moreRead less
The Regulation Of Pluripotency And Self-renewal In Embryonic And Germline Stem Cells.
Funder
National Health and Medical Research Council
Funding Amount
$491,767.00
Summary
Regulation of self-renewal and developmental potential in embryonic and germline stem cells. The capacity of some stem cells to self-renew and under specific conditions, give rise to all adult cell types, a property known as pluripotency , is the key to unlocking the potential of cell based therapies. The development of stem cell based therapies promises to revolutionize the treatment of many common human diseases. For instance, in neurodegenerative conditions such as Parkinsons disease, normal ....Regulation of self-renewal and developmental potential in embryonic and germline stem cells. The capacity of some stem cells to self-renew and under specific conditions, give rise to all adult cell types, a property known as pluripotency , is the key to unlocking the potential of cell based therapies. The development of stem cell based therapies promises to revolutionize the treatment of many common human diseases. For instance, in neurodegenerative conditions such as Parkinsons disease, normal embryonic stem cells grown in culture could be used to replace the lost or disabled neurons in the patient. Many other conditions including diabetes, cystic fibrosis, myocardial infarction (heart attack) and stroke could potentially be treated with stem cell based therapies. Understanding the molecular regulators that govern establishment and maintenance in culture of stem cell lines derived from embryos and from germ cells is the primary goal of this study. We will use well-established techniques to genetically manipulate mouse embryonic stem cells and embryos to examine the role of a specific gene, NANOG. Named after the Celtic legend of Tir NaNog (land of the ever young). When NANOG was forced to remain active, embryonic stem cells were able to grow in media deficient in factors usually required for self-renewal and did not lose their pluripotency even when treated with chemical agents that usually induce differentiation. Understanding the full capacity of NANOG to influence stem cell self-renewal and elucidation of the underlying molecular pathways regulated by this gene will provide valuable insights into the establishment and manipulation of stem cell lines from embryonic and adult tissues.Read moreRead less
Role Of Beta-catenin And Its Regulator FAM In Haemopoietic Stem Cell Function
Funder
National Health and Medical Research Council
Funding Amount
$506,500.00
Summary
Haemopoietic stem cells (HSC) are currently the best characterised adult stem cell (SC) population and currently the only SC population used in cellular therapy. Adult HSC reside in the bone marrow and it is generally accepted that these rare cells cycle slowly and maintain themselves by a process involving self renewal. The cellular physiology that underlies HSC self renewal is still to be defined and no single factor has been described which is able to induce substantial proliferation and expa ....Haemopoietic stem cells (HSC) are currently the best characterised adult stem cell (SC) population and currently the only SC population used in cellular therapy. Adult HSC reside in the bone marrow and it is generally accepted that these rare cells cycle slowly and maintain themselves by a process involving self renewal. The cellular physiology that underlies HSC self renewal is still to be defined and no single factor has been described which is able to induce substantial proliferation and expansion of HSC in a defined system while maintaining critical stem cell properties. Like other SC, a critical characteristic of the rare HSC population of cells is their ability to maintain their unique stem cell properties in vivo (the process of self-renewal) while generating more committed cells which will form large numbers of differentiated and specialized mature blood cells. Recent evidence that HSC can repair other organs under some circumstances raises the possibility that this adult SC population could provide an alternative to embryonic stem cells for many stem cell therapies. If this is the case the therapeutic application of HSC becomes significantly broader. Critical to development of such applications will be an understanding of HSC self renewal and development and new approaches to expand this limited cell population. Major progress in this area will require the definition of both the intrinsic and extrinsic mechanisms that control HSC maintenance and self-renewal. Any findings in this area will have major clinical significance and be of enormous benefit to the community. Here we focus on the role of a known intrinsic regulator of SC behaviour (beta-catenin) with the aim of establishing its role in the maintenance of HSC and its regulation by a novel cofactor (FAM). We will determine if the level of beta-catenin is critical in the maintenance and-or differentiation of haemopoietic stem cells and what role FAM plays in this regulation.Read moreRead less
The Role Of Androgens In Osteoblast Development And Bone Metabolism
Funder
National Health and Medical Research Council
Funding Amount
$64,631.00
Summary
Male hormones are essential for the growth and maintenance of bone in men, but exactly how and when they act on the bone forming cells is unclear. We aim to find out what happens when the target for male hormones (receptor) is removed in the bone forming cells at different stages of their development. This project will increase our understanding of how male hormones regulate bone formation and may assist in the design of new therapies for osteoporosis.
Genomic And Functional Analyses Of A Novel Gene Implicated In Type 1 Diabetes
Funder
National Health and Medical Research Council
Funding Amount
$732,439.00
Summary
We have recently discovered a novel gene that contributes to the development of juvenile diabetes. Unfortunately, very little is known about the function of this gene. To better understand how this gene affects the immune system and contributes to disease, we have generated a unique mouse strain that has a dysfunctional copy of this gene. These mice will enable us to characterise this gene and potentially establish a new area of research in diabetes prevention.
Feeding Behaviour And Obesity Development: Identification Of Novel Intervention Points
Funder
National Health and Medical Research Council
Funding Amount
$923,668.00
Summary
Appetite and food intake is regulated by specific neuronal structures in the brain. The most important area is the hypothalamus from which many neuronal pathways originate to control specific aspects of feeding behaviour and energy usage in the brain and the rest of the body. To better understand the contribution individual neuronal populations make to drive excess food intake we propose a new approach to identify this, making new treatment options for eating disorders and obesity possible.