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Research Topic : gonad development
Scheme : NHMRC Project Grants
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  • Funded Activities (690)
  • Organisations (93)
  • Funded Activity

    An Animal Model To Investigate Normal Kidney And Gonad Development

    Funder
    National Health and Medical Research Council
    Funding Amount
    $186,838.00
    More information
    Funded Activity

    Analysis Of Genes In The Chicken Embryo Which Cause Tes Tis Or Ovaries To Develop

    Funder
    National Health and Medical Research Council
    Funding Amount
    $388,333.00
    More information
    Funded Activity

    The Role Of Inhibin And Related Proteins In Gonadal Dev Elopment

    Funder
    National Health and Medical Research Council
    Funding Amount
    $152,447.00
    More information
    Funded Activity

    How The Developing Reproductive System Becomes Male

    Funder
    National Health and Medical Research Council
    Funding Amount
    $158,852.00
    More information
    Funded Activity

    The Role Of Inhibin In Pregnancy

    Funder
    National Health and Medical Research Council
    Funding Amount
    $135,733.00
    More information
    Funded Activity

    Effects Of Hormones On Sex Differentiation

    Funder
    National Health and Medical Research Council
    Funding Amount
    $148,530.00
    More information
    Funded Activity

    Gonadal Sex Reversal

    Funder
    National Health and Medical Research Council
    Funding Amount
    $425,250.00
    Summary
    Disorders of sexual development are among the most common form of birth defects in humans (1 in 4,000 births) because failure of the gonads to develop does not affect the viability of the individual. Such disorders can have profound psychological and medical consequences upon the individual, family, and society. Some intersexual conditions are the result of inappropriate exposure to hormones during fetal life, and others are due to spontaneous or inherited gene mutation. About 5-10% of ovarian c .... Disorders of sexual development are among the most common form of birth defects in humans (1 in 4,000 births) because failure of the gonads to develop does not affect the viability of the individual. Such disorders can have profound psychological and medical consequences upon the individual, family, and society. Some intersexual conditions are the result of inappropriate exposure to hormones during fetal life, and others are due to spontaneous or inherited gene mutation. About 5-10% of ovarian cancer cases, that affect 1 in 8000 Australian women, are due to the inheritance of a faulty gene. An understanding of the way gene expression and hence tissue differentiation is altered after sex reversal will inform us about the causes and consequences of normal and abnormal sexual development, gonadal malignancies and infertility. The gonad is unusual in that two completely different organs can arise from an essentially identical primordium, so that errors in development lead to intersexual phenotypes. We will use our new experimental animal model to clarify these processes.
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    Funded Activity

    Dissecting The Role Of Hedgehog Signalling In Chondrogenesis And Skeletal Disease

    Funder
    National Health and Medical Research Council
    Funding Amount
    $408,739.00
    Summary
    There are close to 400 inherited disorders that affect how the skeleton develops, as well as a range of injury and age-related skeletal defects. There is much interest in treating such abnormalities with artificial bone grown outside the body. In order to achieve this aim we must understand all of the processes involved in producing and maintaining bone within the body. We are using both mouse and cell culture models of skeletal development to increase our understanding of these processes.
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    Funded Activity

    THE ROLE OF UBIQUITIN LIGASE ADAPTOR PROTEIN NDFIP1 IN NEURONAL DEVELOPMENT

    Funder
    National Health and Medical Research Council
    Funding Amount
    $581,813.00
    Summary
    Many brain diseases are characterized by faulty connections between nerve cells (neurons), in some cases caused by the inability to remove unwanted proteins from the neuron. This function is carried out by the ubiquitin-proteasome system (UPS). We have evidence that a UPS protein called Ndfip1 is important for forming functional brain circuits. We aim to discover whether neuron growth, branching and connectivity is promoted by Ndfip1 targeting of PTEN (phosphatase with tensin homology) to the UP .... Many brain diseases are characterized by faulty connections between nerve cells (neurons), in some cases caused by the inability to remove unwanted proteins from the neuron. This function is carried out by the ubiquitin-proteasome system (UPS). We have evidence that a UPS protein called Ndfip1 is important for forming functional brain circuits. We aim to discover whether neuron growth, branching and connectivity is promoted by Ndfip1 targeting of PTEN (phosphatase with tensin homology) to the UPS.
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    Funded Activity

    Body Segment Identity Specification By The Transcription Regulator, Moz

    Funder
    National Health and Medical Research Council
    Funding Amount
    $366,301.00
    Summary
    One in 28 newborns have birth defects. Cleft palate and aortic arch defects are among the most common, always requiring surgery and often causing lethality. We propose to study a protein, Moz, which is essential for palate and aortic arch development. Moz (Monocytic leukaemia zinc finger protein) was first identified in human chromosomal abnormalities causing particularly aggressive forms of childhood and adult leukaemia. We have shown previously that Moz is essential for the formation of blood .... One in 28 newborns have birth defects. Cleft palate and aortic arch defects are among the most common, always requiring surgery and often causing lethality. We propose to study a protein, Moz, which is essential for palate and aortic arch development. Moz (Monocytic leukaemia zinc finger protein) was first identified in human chromosomal abnormalities causing particularly aggressive forms of childhood and adult leukaemia. We have shown previously that Moz is essential for the formation of blood stem cells. Moz can regulate the activity of genes, but which genes it regulates in vivo is unknown. In the absence of Moz, mice are born with a cleft palate, lack the thymus, where immune cells are instructed, and fail to form the lung blood circulation, so that they are unable to supply their blood with oxygen after birth. Moz deficiency also causes defects of the vertebrate column, such that individual vertebrae acquire the appearance of their neighbours. These symptoms are typical for a general defect in positional information of individual body segments with respect to their location along the body axis. We will investigate the molecular mechanisms that require Moz in patterning of the body axis. This project will characterize a genetic mechanism that is crucial for normal development of the palate, the aorta and the vertebrate column.
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