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Collagen II Mutations And The Unfolded Protein Response In Inherited Cartilage Disease
Funder
National Health and Medical Research Council
Funding Amount
$92,314.00
Summary
In genetic diseases, gene mutations commonly cause proteins to fold abnormally. This can cause cell stress resulting in cell death. My studies will determine the role of cell stress in a clinically important group of diseases, caused by cartilage collagen mutations, that result in abnormal development of the skeleton. These studies will define the mechanisms of how cell stress causes these disorders; knowledge that will underpin the development of new therapeutic strategies
ASSESSMENT OF ENDOPLASMIC RETICULUM STRESS AND MUTATIONS IN MUCIN OLIGOMERIZATION DOMAINS IN ULCERATIVE COLITIS
Funder
National Health and Medical Research Council
Funding Amount
$292,216.00
Summary
Ulcerative colitis affects 0.2% of Australians causing chronic or recurrent health morbidity and affecting employment. In severe cases it is life threatening. Its pathogenesis remains poorly understood. We have exciting and novel preliminary data from humans and informed by our unique animal models that make us propose that the disease is caused by Endoplasmic Reticulum Stress due to misfolding of mucin. We have designed fully powered prospective clinical and lab studies to test this hypothesis.
The Unfolded Protein Response In Inherited Musculoskeletal Disease - Mechanisms And Therapeutic Strategies
Funder
National Health and Medical Research Council
Funding Amount
$643,607.00
Summary
In genetic diseases, gene mutations commonly cause proteins to fold abnormally. This can cause cell stress resulting in cell death. Our studies will determine the role of cell stress in a clinically important group of debilitating inherited bone and cartilage diseases caused by collagen mutations. Our studies will explore the mechanisms of how this stress causes the disease, but importantly will translate these findings by testing a new therapeutic strategy strengthen bones in brittle bone disea ....In genetic diseases, gene mutations commonly cause proteins to fold abnormally. This can cause cell stress resulting in cell death. Our studies will determine the role of cell stress in a clinically important group of debilitating inherited bone and cartilage diseases caused by collagen mutations. Our studies will explore the mechanisms of how this stress causes the disease, but importantly will translate these findings by testing a new therapeutic strategy strengthen bones in brittle bone disease.Read moreRead less
The Unfolded Protein Stress Response In Inherited Skeletal Disease: Mechanism And Therapeutic Strategies
Funder
National Health and Medical Research Council
Funding Amount
$549,092.00
Summary
In genetic diseases, gene mutations commonly cause proteins to fold abnormally. This can cause cell stress resulting in cell death. Our studies will determine the role of cell stress in a clinically important group of skeletal diseases caused by collagen mutations. We will also test how we can use small chemicals to alleviate the damage done to the cells by the misfolded proteins, in the hope that this approach will provide new therapeutic strategies for these disorders.
DETERMINING THE ROLE OF ER STRESS INDUCED APOPTOSIS IN THYMIC NEGATIVE SELECTION
Funder
National Health and Medical Research Council
Funding Amount
$558,189.00
Summary
Apoptosis is an evolutionarily conserved mechanism for killing unwanted cells that are no longer needed, damaged, infected with pathogens or dangerous. Defects in apoptosis can cause a number of diseases. For example, abnormal survival of cells can cause cancer or autoimmune disease. Bim is a protein that induces apoptosis and act as a barrier against cancer and autoimmune diseases. This work is aimed at understanding how Bim acts as a barrier against the development of autoimmunity.
ER Stress-Unfolded Protein Response A Critical Metabolic Pathway For Airway Remodelling In Asthma
Funder
National Health and Medical Research Council
Funding Amount
$789,475.00
Summary
Airway remodelling in asthma is associated with poor clinical outcomes and is not prevented by current treatments. We have found endoplasmic reticulum stress (ERS) and associated unfolded protein response (UPR), a crucial process involve in cellular protein folding, play a key role in airway remodelling in asthma. This study will investigate whether inhibition of ERS prevents goblet cell metaplasia, mucus hypersecretion and fibrosis and can be used as a therapeutic strategy for severe asthma.
The Role Of CYP2E1 In Ethanol-mediated Protein Damage And Its Impact On Proteolytic Processing In The ER
Funder
National Health and Medical Research Council
Funding Amount
$179,239.00
Summary
Alcoholic liver disease (ALD) is the primary factor leading to mortality in chronic alcohol abusers. Alcoholic patients possess antibodies to damaged proteins in their bloodstreams, which indicates an underlying level of oxidative damage is occurring in their livers. The antibodies to these damaged proteins could trigger the destruction of liver cells. Alternatively, the damaged proteins themselves could result in cell death because of the way they are degraded in a particular compartment of the ....Alcoholic liver disease (ALD) is the primary factor leading to mortality in chronic alcohol abusers. Alcoholic patients possess antibodies to damaged proteins in their bloodstreams, which indicates an underlying level of oxidative damage is occurring in their livers. The antibodies to these damaged proteins could trigger the destruction of liver cells. Alternatively, the damaged proteins themselves could result in cell death because of the way they are degraded in a particular compartment of the cell, the endoplasmic reticulum (ER). An enzyme, CYP2E1, has been demonstrated to produce the types of chemicals that damage proteins and it is significantly increased in the liver by alcohol consumption. The current scientific proposal is aimed at determining whether CYP2E1 induction by ethanol contributes to ALD by perturbing the normal cellular disposal of damaged proteins in the ER.Read moreRead less
The Role Of Endoplasmic Reticulum (ER) Stress In Pancreatic Beta-cell Dysfunction.
Funder
National Health and Medical Research Council
Funding Amount
$85,775.00
Summary
Diabetes results from pancreatic ß-cell failure which is characterised by insulin secretory defects and ß-cell destruction. This is mediated by inflammatory cytokines in type 1 diabetes and by high levels of fat in type 2 diabetes. The mechanisms by which ß-cells fail remain to be clarified but they are important considering the current epidemic of diabetes in Australia. This project will enhance our understanding of ß-cell failure and may provide therapeutic targets for diabetes treatment.
Despite the high mortality associated with colon cancer only limited therapy options are available to treat these cancers. Here we propose a new strategy for inhibiting colon cancers driven by a specific type of mutations. Our preliminary data show that loss of DNA encoding a tumor suppressor gene creates a unique vulnerability in colon cancers. The aim of this proposal is to exploit this vulnerability as a strategy for combating colon cancer.