Statements in which the resource exists.
SubjectPredicateObjectContext
pubmed-article:20811452rdf:typepubmed:Citationlld:pubmed
pubmed-article:20811452lifeskim:mentionsumls-concept:C0011065lld:lifeskim
pubmed-article:20811452lifeskim:mentionsumls-concept:C0521390lld:lifeskim
pubmed-article:20811452lifeskim:mentionsumls-concept:C0132173lld:lifeskim
pubmed-article:20811452lifeskim:mentionsumls-concept:C1524003lld:lifeskim
pubmed-article:20811452pubmed:issue7311lld:pubmed
pubmed-article:20811452pubmed:dateCreated2010-9-2lld:pubmed
pubmed-article:20811452pubmed:abstractTextNeurons of the peripheral nervous system have long been known to require survival factors to prevent their death during development. But why they selectively become dependent on secretory molecules has remained a mystery, as is the observation that in the central nervous system, most neurons do not show this dependency. Using engineered embryonic stem cells, we show here that the neurotrophin receptors TrkA and TrkC (tropomyosin receptor kinase A and C, also known as Ntrk1 and Ntrk3, respectively) instruct developing neurons to die, both in vitro and in vivo. By contrast, TrkB (also known as Ntrk2), a closely related receptor primarily expressed in the central nervous system, does not. These results indicate that TrkA and TrkC behave as dependence receptors, explaining why developing sympathetic and sensory neurons become trophic-factor-dependent for survival. We suggest that the expansion of the Trk gene family that accompanied the segregation of the peripheral from the central nervous system generated a novel mechanism of cell number control.lld:pubmed
pubmed-article:20811452pubmed:languageenglld:pubmed
pubmed-article:20811452pubmed:journalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:20811452pubmed:citationSubsetIMlld:pubmed
pubmed-article:20811452pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:20811452pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:20811452pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:20811452pubmed:statusMEDLINElld:pubmed
pubmed-article:20811452pubmed:monthSeplld:pubmed
pubmed-article:20811452pubmed:issn1476-4687lld:pubmed
pubmed-article:20811452pubmed:authorpubmed-author:BardeYves-Ala...lld:pubmed
pubmed-article:20811452pubmed:authorpubmed-author:ZhangLixinLlld:pubmed
pubmed-article:20811452pubmed:authorpubmed-author:LickertHeikoHlld:pubmed
pubmed-article:20811452pubmed:authorpubmed-author:GiallonardoPa...lld:pubmed
pubmed-article:20811452pubmed:authorpubmed-author:RencurelChant...lld:pubmed
pubmed-article:20811452pubmed:authorpubmed-author:BibelMiriamMlld:pubmed
pubmed-article:20811452pubmed:authorpubmed-author:Nikoletopoulo...lld:pubmed
pubmed-article:20811452pubmed:authorpubmed-author:FradeJosé...lld:pubmed
pubmed-article:20811452pubmed:issnTypeElectroniclld:pubmed
pubmed-article:20811452pubmed:day2lld:pubmed
pubmed-article:20811452pubmed:volume467lld:pubmed
pubmed-article:20811452pubmed:ownerNLMlld:pubmed
pubmed-article:20811452pubmed:authorsCompleteYlld:pubmed
pubmed-article:20811452pubmed:pagination59-63lld:pubmed
pubmed-article:20811452pubmed:meshHeadingpubmed-meshheading:20811452...lld:pubmed
pubmed-article:20811452pubmed:meshHeadingpubmed-meshheading:20811452...lld:pubmed
pubmed-article:20811452pubmed:meshHeadingpubmed-meshheading:20811452...lld:pubmed
pubmed-article:20811452pubmed:meshHeadingpubmed-meshheading:20811452...lld:pubmed
pubmed-article:20811452pubmed:meshHeadingpubmed-meshheading:20811452...lld:pubmed
pubmed-article:20811452pubmed:meshHeadingpubmed-meshheading:20811452...lld:pubmed
pubmed-article:20811452pubmed:meshHeadingpubmed-meshheading:20811452...lld:pubmed
pubmed-article:20811452pubmed:meshHeadingpubmed-meshheading:20811452...lld:pubmed
pubmed-article:20811452pubmed:meshHeadingpubmed-meshheading:20811452...lld:pubmed
pubmed-article:20811452pubmed:year2010lld:pubmed
pubmed-article:20811452pubmed:articleTitleNeurotrophin receptors TrkA and TrkC cause neuronal death whereas TrkB does not.lld:pubmed
pubmed-article:20811452pubmed:affiliationBiozentrum, University of Basel, CH-4056 Basel, Switzerland. n.vassiliki@unibas.chlld:pubmed
pubmed-article:20811452pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:20811452pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
entrez-gene:12367entrezgene:pubmedpubmed-article:20811452lld:entrezgene
entrez-gene:18211entrezgene:pubmedpubmed-article:20811452lld:entrezgene
entrez-gene:18212entrezgene:pubmedpubmed-article:20811452lld:entrezgene
entrez-gene:18213entrezgene:pubmedpubmed-article:20811452lld:entrezgene
http://linkedlifedata.com/r...entrezgene:pubmedpubmed-article:20811452lld:entrezgene
http://linkedlifedata.com/r...entrezgene:pubmedpubmed-article:20811452lld:entrezgene
http://linkedlifedata.com/r...entrezgene:pubmedpubmed-article:20811452lld:entrezgene
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:20811452lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:20811452lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:20811452lld:pubmed