Linked Life Data

15820693

Source:http://linkedlifedata.com/resource/pubmed/id/15820693

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2005-4-11
pubmed:abstractText
Ubiquitin-mediated protein degradation has been proposed to play an important role in regulating synaptic transmission. Here we show that LIN-23, the substrate binding subunit of a Skp1/Cullin/F Box (SCF) ubiquitin ligase, regulates the abundance of the glutamate receptor GLR-1 in the ventral nerve cord of C. elegans. Mutants lacking lin-23 had an increased abundance of GLR-1 in the ventral cord. The increase of GLR-1 was not caused by changes in the ubiquitination of GLR-1. Instead, SCF(LIN-23) regulates GLR-1 through the beta-catenin homolog BAR-1 and the TCF/Lef transcription factor homolog POP-1. We hypothesize that LIN-23-mediated degradation of BAR-1 beta-catenin regulates the transcription of Wnt target genes, which in turn alter postsynaptic properties.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0896-6273
pubmed:author
pubmed:issnType
Print
pubmed:day
7
pubmed:volume
46
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
51-64
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
LIN-23-mediated degradation of beta-catenin regulates the abundance of GLR-1 glutamate receptors in the ventral nerve cord of C. elegans.
pubmed:affiliation
Department of Molecular Biology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.