PMID- 10022810
OWN - NLM
STAT- MEDLINE
DCOM- 19990303
LR  - 20161124
IS  - 0950-9232 (Print)
IS  - 0950-9232 (Linking)
VI  - 18
IP  - 6
DP  - 1999 Feb 11
TI  - Expression of the naturally occurring truncated trkB neurotrophin receptor 
      induces outgrowth of filopodia and processes in neuroblastoma cells.
PG  - 1285-96
AB  - We have investigated the effects of the truncated trkB receptor isoform T1 
      (trkB.T1) by transient transfection into mouse N2a neuroblastoma cells. We 
      observed that expression of trkB.T1 leads to a striking change in cell morphology 
      characterized by outgrowth of filopodia and processes. A similar morphological 
      response was also observed in SH-SY5Y human neuroblastoma cells and NIH3T3 
      fibroblasts transfected with trkB.T1. N2a cells lack endogenous expression of 
      trkB isoforms, but express barely detectable amounts of its ligands, 
      brain-derived neurotrophic factor (BDNF) and neurotrophin-4 (NT-4). The 
      morphological change was ligand-independent, since addition of exogenous BDNF or 
      NT-4 or blockade of endogenous trkB ligands did not influence this response. 
      Filopodia and process outgrowth was significantly suppressed when full-length 
      trkB.TK+ was cotransfected together with trkB.T1 and this inhibitory effect was 
      blocked by tyrosine kinase inhibitor K252a. Transfection of trkB.T1 deletion 
      mutants showed that the morphological response is dependent on the extracellular, 
      but not the intracellular domain of the receptor. Our results suggest a novel 
      ligand-independent role for truncated trkB in the regulation of cellular 
      morphology.
FAU - Haapasalo, A
AU  - Haapasalo A
AD  - Laboratory of Molecular Pharmacology, A.I. Virtanen Institute, University of 
      Kuopio, Finland.
FAU - Saarelainen, T
AU  - Saarelainen T
FAU - Moshnyakov, M
AU  - Moshnyakov M
FAU - Arumae, U
AU  - Arumae U
FAU - Kiema, T R
AU  - Kiema TR
FAU - Saarma, M
AU  - Saarma M
FAU - Wong, G
AU  - Wong G
FAU - Castren, E
AU  - Castren E
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Oncogene
JT  - Oncogene
JID - 8711562
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Peptide Fragments)
RN  - 0 (Protein Isoforms)
RN  - 0 (Receptor, Ciliary Neurotrophic Factor)
RN  - 0 (Receptors, Nerve Growth Factor)
RN  - EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
RN  - P658DCA9XD (neurotrophin 4)
SB  - IM
MH  - 3T3 Cells
MH  - Alternative Splicing
MH  - Animals
MH  - Brain Neoplasms/diagnosis
MH  - Brain-Derived Neurotrophic Factor/pharmacology
MH  - Cell Differentiation
MH  - Cell Size
MH  - Genetic Variation
MH  - Humans
MH  - Mice
MH  - Nerve Growth Factors/pharmacology
MH  - Neuroblastoma/*pathology
MH  - Peptide Fragments/biosynthesis/genetics
MH  - Protein Isoforms/biosynthesis/genetics
MH  - Pseudopodia
MH  - Receptor Protein-Tyrosine Kinases/*biosynthesis/genetics
MH  - Receptor, Ciliary Neurotrophic Factor
MH  - Receptors, Nerve Growth Factor/*biosynthesis/genetics
MH  - Sequence Deletion
MH  - Transfection
EDAT- 1999/02/18 00:00
MHDA- 1999/02/18 00:01
CRDT- 1999/02/18 00:00
PHST- 1999/02/18 00:00 [pubmed]
PHST- 1999/02/18 00:01 [medline]
PHST- 1999/02/18 00:00 [entrez]
AID - 10.1038/sj.onc.1202401 [doi]
PST - ppublish
SO  - Oncogene. 1999 Feb 11;18(6):1285-96. doi: 10.1038/sj.onc.1202401.