Linked Life Data

21055464

Source:http://linkedlifedata.com/resource/pubmed/id/21055464

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2011-2-14
pubmed:abstractText
Signaling through the Notch receptor has dramatically different effects depending on cell type and developmental timing. While a myriad of biological systems affected by Notch have been described, the molecular mechanisms by which a generic Notch signal is translated into a cell-type-specific output are less clear. Canonically, the Notch intracellular domain (NICD) translocates into the nucleus upon ligand binding to transcriptionally regulate target genes. In order to generate specificity, therefore, additional factors must exist that modulate NICD activity. Here we describe a novel regulator of the Notch pathway, Endonuclease GI (EndoGI). EndoGI localizes to the nucleus of most cells and activates Notch signaling when overexpressed. In the absence of endoGI, mutant animals are viable, but uncoordinated as motor neurons fail to innervate their appropriate muscle targets. Our data is therefore consistent with EndoGI functioning as a positive regulator of the Notch signaling pathway, playing a critical role during axon guidance of motor neurons.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1872-6356
pubmed:author
pubmed:copyrightInfo
Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
128
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
59-70
pubmed:dateRevised
2011-9-26
pubmed:meshHeading
pubmed:articleTitle
EndoGI modulates Notch signaling and axon guidance in Drosophila.
pubmed:affiliation
Division of Basic Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Av., N. Seattle, WA 98109, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural