Immunocytochemical analysis of phosphatidylinositol-specific phospholipase C in PC12 cells: predominance of the ? isoform during neural differentiation

1993 ◽  
Vol 100 (2) ◽  
pp. 121-129 ◽  
Author(s):  
Luca M. Neri ◽  
Daniela Milani ◽  
Marco Marchisio ◽  
Lucia Bertolaso ◽  
Fiorenzo Marinelli ◽  
...  
1991 ◽  
Vol 266 (3) ◽  
pp. 1359-1362 ◽  
Author(s):  
U H Kim ◽  
D Fink ◽  
H S Kim ◽  
D J Park ◽  
M L Contreras ◽  
...  

Author(s):  
Samira Shariati Najafabadi ◽  
Noushin Amirpour ◽  
Sharhram Amini ◽  
Nasrin Zare ◽  
Mohammad Kazemi ◽  
...  

2002 ◽  
Vol 71 (1) ◽  
pp. 178-185 ◽  
Author(s):  
Sun Sik Bae ◽  
Young Han Lee ◽  
Jong-Soo Chang ◽  
Sehamuddin H. Galadari ◽  
Yong Sik Kim ◽  
...  

2001 ◽  
Vol 21 (8) ◽  
pp. 2695-2705 ◽  
Author(s):  
Deog-Young Choi ◽  
Juan Jose Toledo-Aral ◽  
Rosalind Segal ◽  
Simon Halegoua

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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