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Research Topic : proteolytic cleavage
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  • Researchers (0)
  • Funded Activities (11)
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  • Funded Activity

    Mechanisms Of Endothelin Converting Enzyme Shedding, And Its Role In Cardiovascular Function.

    Funder
    National Health and Medical Research Council
    Funding Amount
    $294,508.00
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    Funded Activity

    Proteolytic Regulation Of Retinoblastoma Protein Function

    Funder
    National Health and Medical Research Council
    Funding Amount
    $74,409.00
    More information
    Funded Activity

    Investigating The Biological Significance Of Proteolytic Prion Protein Processing.

    Funder
    National Health and Medical Research Council
    Funding Amount
    $328,558.00
    Summary
    Prion diseases, including Bovine Spongiform encephalopathy (“mad cow disease”) and Creutzfeldt-Jakob Disease in humans are transmissible and fatal diseases that occur when the normal prion protein (PrPc) mis-folds and accumulates in the brain. The specific function of PrPc within a cell remains unclear, however its presence is essential for prion diseases to occur. This project aims to define how PrPc cleavage affects its biological function(s), and influences susceptibility to prion infection.
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    Funded Activity

    The Effect Of Fluoride On Enamel Formation

    Funder
    National Health and Medical Research Council
    Funding Amount
    $121,975.00
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    Funded Activity

    Pandemic Influenza Vaccine: Exploiting The Conserved HA Cleavage Site

    Funder
    National Health and Medical Research Council
    Funding Amount
    $243,300.00
    Summary
    Influenza virus needs to cleave its surface spike protein, hemagglutinin or HA, to become mature and infectious. This project is aimed at producing a vaccine that will block the cleavage thus rendering the virus non-infectious. To achieve this, we will use synthetic fragments (called peptides) of the viral HA spike protein mimicking its cleavage site to immunize mice. This will produce specific antibodies that will bind to the cleavage site while the virus is inside the infected cell, thus preve .... Influenza virus needs to cleave its surface spike protein, hemagglutinin or HA, to become mature and infectious. This project is aimed at producing a vaccine that will block the cleavage thus rendering the virus non-infectious. To achieve this, we will use synthetic fragments (called peptides) of the viral HA spike protein mimicking its cleavage site to immunize mice. This will produce specific antibodies that will bind to the cleavage site while the virus is inside the infected cell, thus preventing the viral spike protein from being cleaved and remain immature. This idea is particularly suited to fight the bird flu, as all pathogenic bird influenza viruses cleave HA spike proteins within the infected cell.
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    Funded Activity

    Sensitive Detection Of Disease In Leukaemia Patients Af Ter Treatment

    Funder
    National Health and Medical Research Council
    Funding Amount
    $78,968.00
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    Funded Activity

    Identification Of Secretase Responsible For ACE Ectodomain Shedding.

    Funder
    National Health and Medical Research Council
    Funding Amount
    $98,206.00
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    Funded Activity

    Ultraviolet Light Induced Growth Factors: Cell Multipli Cation And Tumour Promotion

    Funder
    National Health and Medical Research Council
    Funding Amount
    $257,246.00
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    Funded Activity

    Proteolytic Processing Of Alzheimer's Amyloid Precursor: Identification Of Gamma-secretase

    Funder
    National Health and Medical Research Council
    Funding Amount
    $240,581.00
    Summary
    Alzheimer's disease is the major cause of dementia among the elderly and affects more than 20% of the population aged 80 and over. There is no cure for the disease and the treatments currently available can only retard its progression and have serious side-effects. Examination of the brain from subjects who died from Alzheimer's disease shows lesions: these are called amyloid plaques. The plaques are formed by the abnormal accumulation of an insoluble and toxic protein which causes death of the .... Alzheimer's disease is the major cause of dementia among the elderly and affects more than 20% of the population aged 80 and over. There is no cure for the disease and the treatments currently available can only retard its progression and have serious side-effects. Examination of the brain from subjects who died from Alzheimer's disease shows lesions: these are called amyloid plaques. The plaques are formed by the abnormal accumulation of an insoluble and toxic protein which causes death of the brain cells. Some gene defects which cause Alzheimer's disease at an early age (30-60 years) are known to accelerate the accumulation of the toxic protein, thereby causing progressive degeneration of the brain. Our research is aimed at understanding at the molecular level how the toxic protein forms. We know that it is part of a large protein and that its release requires two enzyme cuts. Now we propose to isolate and characterize these enzymes and to search for drugs which will neutralize them. This constitutes a rational approach to a therapeutic strategy fo halting or slowing down the progression of Alzheimer's disease.
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    Funded Activity

    Generation Of Beta A4 Amyloid In Alzheimer's Disease

    Funder
    National Health and Medical Research Council
    Funding Amount
    $224,523.00
    More information

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