Linked Life Data

16267171

Source:http://linkedlifedata.com/resource/pubmed/id/16267171

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2005-11-21
pubmed:abstractText
Copper is an essential transition metal but is toxic in excess; therefore, its metabolism needs to be tightly regulated. Defects in the regulation of copper can lead to various disorders characterized by copper deficiency or copper excess. Recently, we characterized the COMMD1 (previously MURR1) gene as the defective gene in canine copper toxicosis. The molecular functions of COMMD1 remain unknown, but significant progress has been made in identifying the cellular processes in which COMMD1 participates, through the identification of proteins interacting with COMMD1. This review discusses how COMMD1 functions as a regulator of not only copper homeostasis but also sodium transport and the NF-kappaB signaling pathway. We outline the possible mechanisms through which COMMD1 exerts these newly identified functions.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0022-1503
pubmed:author
pubmed:issnType
Print
pubmed:volume
96
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
803-11
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
The many faces of the copper metabolism protein MURR1/COMMD1.
pubmed:affiliation
Complex Genetics Section, DBG-Department of Medical Genetics, University Medical Center, 3508 TA Utrecht, The Netherlands.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't