Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1993-11-9
pubmed:abstractText
Neurotrophins are known to have important functions in the survival of embryonic and adult subpopulations of neurons. The identification of Trk family RTKs as receptors for NGF-related neurotrophins indicates phosphotyrosine-mediated signal transduction as a principal mechanism for neurotrophin signaling. Previous trk and trkB expression studies (Klein et al. 1989, 1990b; Martin-Zanca et al. 1990) and more recent studies with trkC (L. Tessarollo et al., in prep.) provide important clues about function. Thus, trkB and trkC expression in motor neurons and in many nonneuronal cells suggests that these cells are targets for neurotrophin action in vivo, even though this has not been demonstrated in the classic in vitro survival assays. Expression of trkB and trkC in nonneuronal cells implies that these receptors may act in additional aspects of organogenesis and development. Current approaches to assay Trk receptor and neurotrophin function will be complemented by further studies in the living organism. Transgenic approaches aimed at ectopic expression and at interfering with normal receptor function should provide additional insights. Finally, reverse genetic approaches using targeted mutation of Trk receptors in embryonic stem cells (Stanton et al. 1992) will allow assessment of critical receptor requirements and provide powerful reagents for studying nervous system development and function.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0091-7451
pubmed:author
pubmed:issnType
Print
pubmed:volume
57
pubmed:geneSymbol
trk, trkB, trkC
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
43-51
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
The Trk family of tyrosine kinases: receptors for NGF-related neurotrophins.
pubmed:affiliation
Molecular Embryology Section, NCI-Frederick Cancer Research and Development Center, Maryland 21702-1201.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.