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A central focus of our research effort is to delineate the molecular mechanisms which control zinc homeostasis. A deficiency of this essential metal is a worldwide health problem. It causes growth retardation, immune system dysfunction, male hypogonadism, skin lesions, and neurological disorders in humans. Maternal zinc deficiency impairs embryonic, fetal and post-natal development ultimately leading to diminished reproductive success and a plethora of health problems in the offspring. It has also recently been shown that zinc influences signal transduction cascades within cells and can increase the metastatic potential of cancer cells.
To understand more about mechanisms of zinc homeostasis we are currently studying the structure, function and regulation of a newly identified family of zinc transporter genes. One of these genes called Zip4 causes the rare, autosomal recessive human disorder acrodermatitis enteropathica, which reflects an impaired ability to absorb sufficient dietary zinc. Symptoms of severe nutritional zinc deficiency often develop soon after birth and without treatment these children die. We have cloned the Zip4 gene and are mutating it in mice in order to provide a mouse model of this devastating disease and to delineate the tissue-specific functions of this protein. We have also discovered that the expression of this gene and protein are tightly regulated and we are exploring the molecular mechanisms involved.
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Social Science Research Network (2019)
mag(2015)
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