Linked Life Data

10561691

Source:http://linkedlifedata.com/resource/pubmed/id/10561691

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2000-1-5
pubmed:abstractText
FE65 is predominantly expressed in brain and is especially rich in the regions with the highest densities of neurons. The FE65 protein binds to an intracellular domain of the beta-amyloid precursor protein (betaPP) and may modulate the production of beta-amyloid peptide (AP). One of FE65 exons, a mini-exon (exon 9, 6 bp), is alternatively spliced, giving rise to two isoforms varying only in 6 base pairs. We quantitated the two isoforms by a sensitive reverse transcription-competitive polymerase chain reaction technique, and characterized their expressions in various tissues and cell cultures, and the kinetics of expression of the two isoforms in P19 embryonal carcinoma cell lines during neuronal differentiation. Our results show that the exon 9-inclusive (E9) form, the more abundant form in brain, was exclusively expressed in neurons, while the exon 9-exclusive (DeltaE9) form was widely expressed in all non-neuronal cells, but was not expressed in differentiated neurons. When P19 cells were differentiated to neurons, expression of FE65 was significantly up regulated ( approximately 30-fold) and the splicing pattern of the FE65 pre-mRNA was switched from the DeltaE9 pattern to the E9 form. Based upon their distinctive expression patterns, these two isoforms may serve as neuronal and non-neuronal markers, and determination of their ratios may have applications in neuropathological diagnosis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0360-4012
pubmed:author
pubmed:copyrightInfo
Copyright 1999 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
58
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
632-40
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Alternatively spliced isoforms of FE65 serve as neuron-specific and non-neuronal markers.
pubmed:affiliation
Department of Pathology, University of Washington, Seattle, USA. qhu@u.washington.ed
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't