Linked Life Data

18761103

Source:http://linkedlifedata.com/resource/pubmed/id/18761103

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2009-2-23
pubmed:abstractText
As the trace element copper is essential, but extremely toxic in high concentrations, intracellular copper concentrations are tightly controlled. Once in the cell, copper is distributed by metallochaperones, including the small cytoplasmic protein ATOX1. ATOX1 plays an important role in the transfer of copper to the copper export P-type ATPases ATP7A and ATP7B to facilitate copper excretion. Recently, a novel function for Atox1 as a transcription factor (TF) regulating Ccnd1 was proposed. Crystal structures of ATOX1 reveal copper-dependent homodimerization of ATOX1. As many TFs regulate gene expression as a dimer and bind to DNA repeats, we investigated the promotor region of CCND1 and detected a direct repeat sequence in the Atox1 binding site (tentatively referred to as CABE, copper-responsive Atox1 binding element). We therefore propose copper-dependent homodimerization to be an essential step in the regulation of ATOX1-dependent transcription.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1878-5875
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
41
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1233-6
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
ATOX1: a novel copper-responsive transcription factor in mammals?
pubmed:affiliation
Laboratory for Metabolic and Endocrine Diseases, UMC Utrecht, Lundlaan 6, 3584 EA Utrecht, The Netherlands.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't