PMID- 10561691
OWN - NLM
STAT- MEDLINE
DCOM- 20000105
LR  - 20191103
IS  - 0360-4012 (Print)
IS  - 0360-4012 (Linking)
VI  - 58
IP  - 5
DP  - 1999 Dec 1
TI  - Alternatively spliced isoforms of FE65 serve as neuron-specific and non-neuronal 
      markers.
PG  - 632-40
AB  - 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.
CI  - Copyright 1999 Wiley-Liss, Inc.
FAU - Hu, Q
AU  - Hu Q
AD  - Department of Pathology, University of Washington, Seattle, USA. 
      qhu@u.washington.ed
FAU - Hearn, M G
AU  - Hearn MG
FAU - Jin, L W
AU  - Jin LW
FAU - Bressler, S L
AU  - Bressler SL
FAU - Martin, G M
AU  - Martin GM
LA  - eng
GR  - AG05136-15/AG/NIA NIH HHS/United States
GR  - AG10917-07/AG/NIA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (APBB1 protein, human)
RN  - 0 (Apbb1 protein, mouse)
RN  - 0 (Biomarkers)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Nuclear Proteins)
RN  - 0 (Protein Isoforms)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Alternative Splicing/*genetics
MH  - Animals
MH  - Biomarkers
MH  - Brain Chemistry/genetics
MH  - Exons
MH  - Female
MH  - Gene Expression Regulation
MH  - Humans
MH  - Mice
MH  - Nerve Tissue Proteins/*genetics
MH  - Neurons/*chemistry
MH  - Nuclear Proteins/*genetics
MH  - Protein Isoforms/genetics
MH  - RNA, Messenger/analysis
MH  - Tumor Cells, Cultured
EDAT- 1999/11/24 00:00
MHDA- 1999/11/24 00:01
CRDT- 1999/11/24 00:00
PHST- 1999/11/24 00:00 [pubmed]
PHST- 1999/11/24 00:01 [medline]
PHST- 1999/11/24 00:00 [entrez]
AID - 10.1002/(SICI)1097-4547(19991201)58:5<632::AID-JNR4>3.0.CO;2-P [pii]
AID - 10.1002/(sici)1097-4547(19991201)58:5<632::aid-jnr4>3.0.co;2-p [doi]
PST - ppublish
SO  - J Neurosci Res. 1999 Dec 1;58(5):632-40. doi: 
      10.1002/(sici)1097-4547(19991201)58:5<632::aid-jnr4>3.0.co;2-p.