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  • Funded Activities (15)
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  • Funded Activity

    Control Of CD4 Function By Disulphide-Bond Switching

    Funder
    National Health and Medical Research Council
    Funding Amount
    $252,761.00
    Summary
    CD4 is a cell-surface protein that has two functions in the human body, a good one and a bad one. Its good function is as a checkpoint for development of the immune system and for response of the immune system to infection. It helps immune cells known as T cells to recognize and dispose of a foreign particle in the body. Its bad function is that it is one of two proteins that enable the HIV virus to enter and destroy immune cells. The HIV virus binds to CD4 on immune cells, which leads to fusion .... CD4 is a cell-surface protein that has two functions in the human body, a good one and a bad one. Its good function is as a checkpoint for development of the immune system and for response of the immune system to infection. It helps immune cells known as T cells to recognize and dispose of a foreign particle in the body. Its bad function is that it is one of two proteins that enable the HIV virus to enter and destroy immune cells. The HIV virus binds to CD4 on immune cells, which leads to fusion of the viral and immune cell surfaces and entry of the virus into the cell. Once inside the immune cell the virus reproduces itself and goes on to kill more immune cells. AIDS results when too many immune cells are killed. We have discovered that CD4 exists in three different forms on the immune cell surface; an oxidized, reduced or dimeric form. These different forms result from a molecular switch we discovered in CD4. We have suggested that the good and bad functions of CD4 are mediated by different forms of CD4. The good function is mediated by dimeric CD4, while the bad function is mediated by reduced CD4. The purpose of this application is to test this hypothesis. If we are correct then our findings will have significant implications for our understanding of how the immune system responds to a foreign invader and how HIV-AIDS destroys the immune system. This knowledge could be used to develop drugs that suppress the immune system when required, such as in organ transplantation, and that fight HIV-AIDS.
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    Funded Activity

    Role Of HIV-1 P6 Late Domain In Virus Budding And Release.

    Funder
    National Health and Medical Research Council
    Funding Amount
    $390,018.00
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    Funded Activity

    A Transgenic Analysis Of The Basis For Growth Signalling By The Growth Hormone Receptor

    Funder
    National Health and Medical Research Council
    Funding Amount
    $209,455.00
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    Funded Activity

    Signalling Cell Death - Structural Basis Of Death Effector/adaptor Recruitment

    Funder
    National Health and Medical Research Council
    Funding Amount
    $283,768.00
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    Funded Activity

    A Transgenic Analysis Of The Basis For Growth Signalling By The Growth Hormone Receptor

    Funder
    National Health and Medical Research Council
    Funding Amount
    $45,816.00
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    Funded Activity

    Biochemical & Physiological Characterisation Of The SPRY-domain Containing SOCS Box (SSB) Proteins

    Funder
    National Health and Medical Research Council
    Funding Amount
    $444,500.00
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    Funded Activity

    Studies Of A Third EGF-domain Containing Merozoite Protein Of Plasmodium Falciparum

    Funder
    National Health and Medical Research Council
    Funding Amount
    $172,166.00
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    Funded Activity

    Role Of A Clotting Protein In The Control Of Bleeding

    Funder
    National Health and Medical Research Council
    Funding Amount
    $121,457.00
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    Funded Activity

    Mechanisms Of SQ/TQ Cluster Domain Function In DNA Damage Response

    Funder
    National Health and Medical Research Council
    Funding Amount
    $293,250.00
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    Funded Activity

    Molecular Genetic Analysis Of BRCT Domain Function And RhoGEF Signalling In DNA-damage Response And Apoptosis.

    Funder
    National Health and Medical Research Council
    Funding Amount
    $195,691.00
    Summary
    Cancers arise as a consequence of a series of genetic changes, usually by mutation of DNA. DNA is consistently exposed to an array of damaging agents, but the majority of mutations are corrected by cellular repair mechanisms. We now know that if these mechanisms work normally, too few mutations persist for cancer to result. However if these DNA damage repair mechanisms are themselves faulty, a high mutation rate occurs and a high risk of cancer results. DNA damage has another outcome. If the dam .... Cancers arise as a consequence of a series of genetic changes, usually by mutation of DNA. DNA is consistently exposed to an array of damaging agents, but the majority of mutations are corrected by cellular repair mechanisms. We now know that if these mechanisms work normally, too few mutations persist for cancer to result. However if these DNA damage repair mechanisms are themselves faulty, a high mutation rate occurs and a high risk of cancer results. DNA damage has another outcome. If the damage is too extensive, the cell commits suicide, not because it cannot function, but because it senses the DNA damage and chooses to die. One poorly understood aspect of the response to DNA damage is how the cell senses the damage and activates the suicide process. We have discovered a novel gene that appears to play a role in this sensing and suicide signalling process. The mouse version of this gene can itself act as a cancer-causing gene. We propose, however, to study the equivalent gene in Drosophila melanogaster, a more powerful experimental system, to characterise in detail its role in these processes. In this way we hope to generate a much more detailed understanding of the way that cells deal with DNA damage and choose suicide when the damage is too severe.
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