Copper toxicosis gene MURR1 is not changed in Wilson disease patients with normal blood ceruloplasmin levels
نویسندگان
چکیده
منابع مشابه
Identification of a new copper metabolism gene by positional cloning in a purebred dog population.
Domesticated animal species such as dogs and cats, with their many different characteristics and breed-specific diseases, and their close relationship and shared environment with humans, are a potentially rich source for the identification of the genetic contribution to human biology and disease. Copper toxicosis in Bedlington terriers is a genetic disease occurring with a high prevalence world...
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Bacground: Wilson's disease is a rare autosomal recessive disorder characterized by toxic accumulation of copper in liver and brain. The disorder is caused by mutations in the ATP7B gene, encoding a copper transporting P-type ATPase. Characterization of the spectrum of mutations in this gene is important both for diagnosis and genetic counseling of the families. Materials and Methods: We enrol...
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Although periodontitis is a chronic inflammatory disease but some factors of acute inflammation phase are involved in this disease among which is the C-Reactive protein (CRP). To minimize its effects, anti-inflammatory drugs or non-pharmacological approaches such as oral hygiene is recommended. CRP can also be used for the prediction and early detection of periodontal disease. The aim of the pr...
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چکیده ندارد.
15 صفحه اولXIAP Is a copper binding protein deregulated in Wilson's disease and other copper toxicosis disorders.
X-linked inhibitor of apoptosis (XIAP), known primarily for its caspase inhibitory properties, has recently been shown to interact with and regulate the levels of COMMD1, a protein associated with a form of canine copper toxicosis. Here, we describe a role for XIAP in copper metabolism. We find that XIAP levels are greatly reduced by intracellular copper accumulation in Wilson's disease and oth...
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ژورنال
عنوان ژورنال: World Journal of Gastroenterology
سال: 2006
ISSN: 1007-9327
DOI: 10.3748/wjg.v12.i14.2239