
DOI . ORG {
}
Title[redir]:
Wilson disease: New insights into pathogenesis, diagnosis, and future therapy | Current Gastroenterology Reports
Description:
Wilson disease is caused by disease-specific mutations of the copper transporting ATPase, ATP7B. The diagnosis is established by clinical and biochemical means, though advances in molecular diagnostics will someday permit de novo diagnosis. The patient may present with hepatic, neurologic, or psychiatric symptoms, or a combination of these. Both environmental and extragenic effects contribute to the varied phenotypic presentations of this disease. Patients can be treated effectively with chelating agents or zinc salts, or with liver transplantation. Liver cell transplant and gene therapy offer potential cures for this disorder, but at present only data from preclinical studies on animal models are available. Future advances in immunotolerization and gene therapy will likely enable human trials for treatment of this disorder and other genetic disorders of hepatic metabolism.
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Keywords {π}
disease, article, google, scholar, pubmed, wilson, cas, copper, gene, liver, wilsons, atpb, lec, rats, hepatic, transplantation, genet, gastroenterology, phenotypic, hum, rat, expression, privacy, cookies, content, data, diagnosis, schilsky, cell, studies, menkes, toxicosis, normal, function, analysis, publish, search, therapy, mutations, patients, human, access, biochem, model, demonstrated, correction, information, log, journal, research,
Topics {βοΈ}
n-terminal metal-binding sites crigler-najjar syndrome type month download article/chapter long-evans cinnamon rats vivo site-directed mutagenesis chimeric rna/dna oligonucleotides udp-glucuronosyltransferase gene defect hepatocellular copper metabolism copper transporting atpase full article pdf human liver cdna privacy choices/manage cookies hepatic metabolism prevent copper toxicosis article schilsky normal liver cells hepatic gene correction liver cell lines wilson disease gene copper metabolic pathway van de sluis factor ix gene liver cell transplant wilson disease locus biliary copper excretion kren bt hepatic copper disease-specific mutants disease protein plays copper transport defect menkes patient fibroblasts rats successfully transplanted normal rat hepatocytes european economic area related subjects gitlin jd defective cellular localization proper cellular localization genotype-phenotype correlation alter gene expression human wilson protein hepatoma cell lines enable human trials conditions privacy policy endosomal/lysosomal vesicles iron overload disorders achieve selective repopulation wilson disease patients future therapy published varied phenotypic presentations
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headline:Wilson disease: New insights into pathogenesis, diagnosis, and future therapy
description:Wilson disease is caused by disease-specific mutations of the copper transporting ATPase, ATP7B. The diagnosis is established by clinical and biochemical means, though advances in molecular diagnostics will someday permit de novo diagnosis. The patient may present with hepatic, neurologic, or psychiatric symptoms, or a combination of these. Both environmental and extragenic effects contribute to the varied phenotypic presentations of this disease. Patients can be treated effectively with chelating agents or zinc salts, or with liver transplantation. Liver cell transplant and gene therapy offer potential cures for this disorder, but at present only data from preclinical studies on animal models are available. Future advances in immunotolerization and gene therapy will likely enable human trials for treatment of this disorder and other genetic disorders of hepatic metabolism.
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Menkes Disease
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headline:Wilson disease: New insights into pathogenesis, diagnosis, and future therapy
description:Wilson disease is caused by disease-specific mutations of the copper transporting ATPase, ATP7B. The diagnosis is established by clinical and biochemical means, though advances in molecular diagnostics will someday permit de novo diagnosis. The patient may present with hepatic, neurologic, or psychiatric symptoms, or a combination of these. Both environmental and extragenic effects contribute to the varied phenotypic presentations of this disease. Patients can be treated effectively with chelating agents or zinc salts, or with liver transplantation. Liver cell transplant and gene therapy offer potential cures for this disorder, but at present only data from preclinical studies on animal models are available. Future advances in immunotolerization and gene therapy will likely enable human trials for treatment of this disorder and other genetic disorders of hepatic metabolism.
datePublished:
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pageEnd:31
sameAs:https://doi.org/10.1007/s11894-005-0062-5
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