PMID- 10486198
OWN - NLM
STAT- MEDLINE
DCOM- 19991007
LR  - 20161124
IS  - 0014-4886 (Print)
IS  - 0014-4886 (Linking)
VI  - 159
IP  - 1
DP  - 1999 Sep
TI  - Early BDNF, NT-3, and NT-4 signaling events.
PG  - 297-308
AB  - Much more is known about nerve growth factor (NGF) signaling than that initiated 
      by brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), or NT-4. We
      sought to study early BDNF, NT-3, and NT-4 signaling events. Using
      TrkB-expressing cells, we found that BDNF and NT-4 individually induced tyrosine 
      phosphorylation of TrkB in a dose-dependent fashion. At maximally effective
      concentrations, BDNF or NT-4 induced robust TrkB tyrosine phosphorylation at 5
      min; this progressively declined at 15, 30, and 60 min. Using
      immunoprecipitation, PI3-kinase and tyrosine phosphorylated PLC-gamma1 and SHC
      were shown to be associated with tyrosine phosphorylated TrkB in response to both
      BDNF and NT-4. BDNF and NT-4 induced similar intensities of phosphorylation of
      TrkB and signaling intermediates at equivalent doses. NT-3 treatment of
      TrkC-expressing cells induced very similar patterns for induction of TrkC
      tyrosine phosphorylation and recruitment of signaling intermediates. BDNF, NT-3, 
      and NT-4 caused rapid tyrosine phosphorylation of ERK and SNT. These data suggest
      that the earliest signaling events for BDNF, NT-3, and NT-4 are very similar to
      those for NGF.
CI  - Copyright 1999 Academic Press.
FAU - Yuen, E C
AU  - Yuen EC
AD  - Department of Neurology, University of Washington, Seattle, Washington, 98195,
      USA.
FAU - Mobley, W C
AU  - Mobley WC
LA  - eng
GR  - AG00649/AG/NIA NIH HHS/United States
GR  - NS24054/NS/NINDS 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  - Exp Neurol
JT  - Experimental neurology
JID - 0370712
RN  - 0 (Adaptor Proteins, Signal Transducing)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (FRS2 protein, human)
RN  - 0 (Isoenzymes)
RN  - 0 (Membrane Proteins)
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Neurotrophin 3)
RN  - 0 (Phosphoproteins)
RN  - 0 (Receptor, Ciliary Neurotrophic Factor)
RN  - 0 (Receptors, Nerve Growth Factor)
RN  - 42HK56048U (Tyrosine)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
RN  - EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
RN  - EC 2.7.10.1 (Receptor, trkC)
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinases)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - EC 3.1.4.- (Type C Phospholipases)
RN  - EC 3.1.4.3 (Phospholipase C gamma)
RN  - P658DCA9XD (neurotrophin 4)
SB  - IM
MH  - 3T3 Cells/chemistry/physiology
MH  - Adaptor Proteins, Signal Transducing
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/pharmacology
MH  - Calcium-Calmodulin-Dependent Protein Kinases/metabolism
MH  - Dose-Response Relationship, Drug
MH  - Gene Expression/physiology
MH  - Humans
MH  - Isoenzymes/metabolism
MH  - Membrane Proteins/metabolism
MH  - Mice
MH  - Mitogen-Activated Protein Kinase 3
MH  - *Mitogen-Activated Protein Kinases
MH  - Nerve Growth Factors/*pharmacology
MH  - Neuroprotective Agents/pharmacology
MH  - Neurotrophin 3
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Phospholipase C gamma
MH  - Phosphoproteins/metabolism
MH  - Phosphorylation
MH  - Receptor Protein-Tyrosine Kinases/metabolism
MH  - Receptor, Ciliary Neurotrophic Factor
MH  - Receptor, trkC
MH  - Receptors, Nerve Growth Factor/metabolism
MH  - Signal Transduction/*drug effects/*physiology
MH  - Transfection
MH  - Type C Phospholipases/metabolism
MH  - Tyrosine/metabolism
MH  - src Homology Domains/physiology
EDAT- 1999/09/16 00:00
MHDA- 1999/09/16 00:01
CRDT- 1999/09/16 00:00
PHST- 1999/09/16 00:00 [pubmed]
PHST- 1999/09/16 00:01 [medline]
PHST- 1999/09/16 00:00 [entrez]
AID - 10.1006/exnr.1999.7148 [doi]
AID - S0014-4886(99)97148-0 [pii]
PST - ppublish
SO  - Exp Neurol. 1999 Sep;159(1):297-308. doi: 10.1006/exnr.1999.7148.