PMID- 10533983
OWN - NLM
STAT- MEDLINE
DCOM- 19991116
LR  - 20161124
IS  - 1079-9893 (Print)
IS  - 1079-9893 (Linking)
VI  - 19
IP  - 6
DP  - 1999 Nov
TI  - The TrkB receptor tyrosine kinase regulates cellular proliferation via signal 
      transduction pathways involving SHC, PLCgamma, and CBL.
PG  - 953-74
AB  - The TrkB protein tyrosine kinase is a high affinity receptor for brain derived 
      neurotrophic factor (BDNF) and neurotrophin-4 (NT-4). TrkB autophosphorylation 
      occurs on five cytoplasmic tyrosines: Y484, Y670, Y674, Y675, and Y785. Using 
      site directed mutagenesis, we have assessed the importance of TrkB tyrosines 484 
      and 785 in affecting TrkB-mediated signaling events leading to NIH 3T3 cell 
      mitogenesis and survival. Mutation of TrkB tyrosine 484, while having no affect 
      on BDNF-inducible PLCgamma and Cbl tyrosine phosphorylation, is essential for the 
      phosphorylation of Shc, the complete activation of extracellular regulated kinase 
      1/2 (ERK1/2) and the induction of c-fos protein synthesis. In contrast, mutation 
      of Y785 does not significantly affect BDNF-inducible Shc phosphorylation, ERK1/2 
      activation, or c-fos protein synthesis, but completely inhibits the tyrosine 
      phosphorylation of PLCgamma and Cbl. These data indicate that both ERK-dependent 
      and ERK-independent signaling pathways lead to BDNF-inducible mitogenesis and 
      survival.
FAU - McCarty, J H
AU  - McCarty JH
AD  - Department of Molecular, Cellular and Developmental Biology and Neuroscience 
      Research Institute, University of California, Santa Barbara 93106, USA.
FAU - Feinstein, S C
AU  - Feinstein SC
LA  - eng
GR  - EY10739/EY/NEI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - J Recept Signal Transduct Res
JT  - Journal of receptor and signal transduction research
JID - 9509432
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Isoenzymes)
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Oncogene Protein v-cbl)
RN  - 0 (Retroviridae Proteins, Oncogenic)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - EC 3.1.4.- (Type C Phospholipases)
RN  - EC 3.1.4.3 (Phospholipase C gamma)
RN  - EC 5.4.- (Intramolecular Transferases)
RN  - EC 5.4.99.- (squalene-hopene cyclase)
RN  - P658DCA9XD (neurotrophin 4)
SB  - IM
MH  - 3T3 Cells
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/physiology
MH  - Cell Division/physiology
MH  - Intramolecular Transferases/*physiology
MH  - Isoenzymes/*physiology
MH  - Mice
MH  - Mutagenesis, Site-Directed
MH  - Nerve Growth Factors/physiology
MH  - Oncogene Protein v-cbl
MH  - Phospholipase C gamma
MH  - Phosphorylation
MH  - Rats
MH  - Receptor, trkB/*physiology
MH  - Retroviridae Proteins, Oncogenic/*physiology
MH  - *Signal Transduction/physiology
MH  - Type C Phospholipases/*physiology
EDAT- 1999/10/26 00:00
MHDA- 1999/10/26 00:01
CRDT- 1999/10/26 00:00
PHST- 1999/10/26 00:00 [pubmed]
PHST- 1999/10/26 00:01 [medline]
PHST- 1999/10/26 00:00 [entrez]
AID - 10.3109/10799899909038434 [doi]
PST - ppublish
SO  - J Recept Signal Transduct Res. 1999 Nov;19(6):953-74. doi: 
      10.3109/10799899909038434.