Identification and Structure of the Nerve Growth Factor Binding Site on TrkA

2001 ◽  
Vol 282 (1) ◽  
pp. 131-141 ◽  
Author(s):  
Alan G.S. Robertson ◽  
Mark J. Banfield ◽  
Shelley J. Allen ◽  
Julie A. Dando ◽  
Grant G.F. Mason ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Binding Site ◽  
Nerve Growth ◽  
Factor Binding Site ◽  
Factor Binding

Immunoglobulin-like domains define the nerve growth factor binding site of the TrkA receptor

1997 ◽  
Vol 15 (7) ◽  
pp. 668-672 ◽  
Author(s):  
Paul H. Holden ◽  
Vipin Asopa ◽  
Alan G.S. Robertson ◽  
Anthony R. Clarke ◽  
Sue Tyler ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Binding Site ◽  
Trka Receptor ◽  
Nerve Growth ◽  
Factor Binding Site ◽  
Factor Binding

scholarly journals Nerve Growth Factor Binding Site on TrkA Mapped to a Single 24-Amino Acid Leucine-rich Motif

1995 ◽  
Vol 270 (47) ◽  
pp. 28133-28138 ◽  
Author(s):  
Jörg M. Windisch ◽  
Rainer Marksteiner ◽  
Rainer Schneider
Keyword(s):  
Amino Acid ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Binding Site ◽  
Nerve Growth ◽  
Factor Binding Site ◽  
Factor Binding

Nerve growth factor binding sites on hepatic parenchymal cells

1992 ◽  
Vol 28 (9-10) ◽  
pp. 621-624 ◽  
Author(s):  
M. B. Bailie ◽  
R. A. Roth ◽  
M. L. Contreras
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Binding Sites ◽  
Nerve Growth ◽  
Factor Binding ◽  
Parenchymal Cells

scholarly journals Sustained Signaling by Phospholipase C-γ Mediates Nerve Growth Factor-Triggered Gene Expression

2001 ◽  
Vol 21 (8) ◽  
pp. 2695-2705 ◽  
Author(s):  
Deog-Young Choi ◽  
Juan Jose Toledo-Aral ◽  
Rosalind Segal ◽  
Simon Halegoua
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Binding Site ◽  
Phospholipase C ◽  
Pc12 Cells ◽  
Nerve Growth ◽  
Neuronal Gene ◽  
Intracellular Ca ◽  
Kinetics Of

ABSTRACT In contrast to conventional signaling by growth factors that requires their continual presence, a 1-min pulse of nerve growth factor (NGF) is sufficient to induce electrical excitability in PC12 cells due to induction of the peripheral nerve type 1 (PN1) sodium channel gene. We have investigated the mechanism for this triggered signaling pathway by NGF in PC12 cells. Mutation of TrkA at key autophosphorylation sites indicates an essential role for the phospholipase C-γ (PLC-γ) binding site, but not the Shc binding site, for NGF-triggered induction of PN1. In concordance with results with Trk mutants, drug-mediated inhibition of PLC-γ activity also blocks PN1 induction by NGF. Examination of the kinetics of TrkA autophosphorylation indicates that triggered signaling does not result from sustained activation and autophosphorylation of the TrkA receptor kinase, whose phosphorylation state declines rapidly after NGF removal. Rather, TrkA triggers an unexpectedly prolonged phosphorylation and activation of PLC-γ signaling that is sustained for up to 2 h. Prevention of the elevation of intracellular Ca2+ levels using BAPTA-AM results in a block of PN1 induction by NGF. Sustained signaling by PLC-γ provides a means for differential neuronal gene induction after transient exposure to NGF.

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