Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2011-8-8
pubmed:abstractText
The delta subunit of the epithelial sodium channel (?ENaC) is a member of the ENaC/degenerin family of ion channels. ?ENaC is distinct from the related ?-, ?- and ?ENaC subunits, known for their role in sodium homeostasis and blood pressure control, as ?ENaC is expressed in brain neurons and activated by external protons. COMMD1 (copper metabolism Murr1 domain 1) was previously found to associate with and downregulate ?ENaC activity. Here, we show that COMMD1 interacts with ?ENaC through its COMM domain. Co-expression of ?ENaC with COMMD1 significantly reduced ?ENaC surface expression, and led to an increase in ?ENaC ubiquitination. Immunocytochemical and confocal microscopy studies show that COMMD1 promoted localization of ?ENaC to the early/recycling endosomal pool where the two proteins were localized together. These results suggest that COMMD1 downregulates ?ENaC activity by reducing ?ENaC surface expression through promoting internalization of surface ?ENaC to an intracellular recycling pool, possibly via enhanced ubiquitination.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1090-2104
pubmed:author
pubmed:copyrightInfo
Copyright © 2011 Elsevier Inc. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
5
pubmed:volume
411
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
506-11
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
COMMD1 regulates the delta epithelial sodium channel (?ENaC) through trafficking and ubiquitination.
pubmed:affiliation
Department of Physiology, University of Otago, PO Box 913, Dunedin 9054, New Zealand.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't