Protein Kinase C Mediates Short-and Long-term Effects on Receptor Tyrosine Kinases.

1995 ◽  
Vol 766 (1 Receptor Acti) ◽  
pp. 459-462 ◽  
Author(s):  
KLAUS SEEDORF ◽  
MARK SHERMAN ◽  
AXEL ULLRICH
1993 ◽  
Vol 69 (2) ◽  
pp. 636-641 ◽  
Author(s):  
T. Crow ◽  
J. Forrester

1. The visual system of Hermissenda has been studied extensively as a site of cellular plasticity produced by classical conditioning. Previous research has shown that one-trial conditioning, consisting of light paired with serotonin (5-HT) results in short- and long-term enhancement of light-elicited generator potentials in identified type B-photoreceptors. Recent evidence suggests that 5-HT exerts its effects on the induction of short-term enhancement by activation of protein kinase C (PKC), a Ca(2+)-activated and phospholipid-dependent protein kinase. However, the contribution of protein kinases in general, and specifically PKC in long-term enhancement has not been established. 2. The protein kinase inhibitors H-7 and sphingosine blocked the induction of short-term enhancement when applied before one-trial conditioning. However, the conditions that are sufficient to block the induction of short-term enhancement do not block long-term enhancement. Sphingosine and H-7 do not block the induction and expression of long-term enhancement when applied before one-trial conditioning. 3. Pretreatment before conditioning with 12-O-tetradecanoyl-phorbol-13-acetate (TPA), which leads to down-regulation of PKC, also did not block long-term enhancement. Down-regulation by itself did not produce enhancement, although the transient peak of light-elicited generator potentials was reduced by pretreatment with TPA. 4. The results suggest that the induction of short- and long-term enhancement involve parallel processes, and thus the expression of long-term cellular plasticity produced by one-trial conditioning does not depend on the induction or expression of short-term enhancement.


1999 ◽  
Vol 274 (49) ◽  
pp. 34691-34698 ◽  
Author(s):  
Matthias Voß ◽  
Paschal A. Oude Weernink ◽  
Stephan Haupenthal ◽  
Ursula Möller ◽  
Robbert H. Cool ◽  
...  

1988 ◽  
Vol 12 ◽  
pp. 73-79 ◽  
Author(s):  
Doriano Fabbro ◽  
Nachman Mazurek ◽  
Christoph Borner ◽  
Jean-François Conscience ◽  
Paul Erne

2002 ◽  
Vol 22 (9) ◽  
pp. 2928-2938 ◽  
Author(s):  
Peihong Ma ◽  
Maureen Magut ◽  
XinBin Chen ◽  
Chang-Yan Chen

ABSTRACT The tumor suppressor p53 eliminates cancer-prone cells via multiple mechanisms, including apoptosis. Ras elicits apoptosis in cells after protein kinase C (PKC) downregulation. However, the role of p53 in Ras-mediated apoptosis has not been fully investigated. Here, we demonstrate that mouse fibroblasts that express wild-type p53 are more susceptible to apoptosis elicited by PKC inhibition if Ras is transiently expressed or upregulated as opposed to stably expressed. In the latter case, p53 is frequently mutated. Transiently increased Ras activity induces Bax, and PKC inhibition augments this induction. Overexpression of E6 inactivates p53 and thereby suppresses both Bax induction and apoptosis. In contrast, Bax is not induced in stable ras transfectants, regardless of PKC inhibition. The data suggest that short- and long-term activation of Ras use a different mechanism(s) to initiate apoptosis. The status of p53 may contribute to such differences.


1988 ◽  
Vol 12 (Supplement) ◽  
pp. 73-79
Author(s):  
Doriano Fabbro ◽  
Nachman Mazurek ◽  
Christoph Borner ◽  
Jean-François Conscience ◽  
Paul Erne

Nature ◽  
1987 ◽  
Vol 328 (6129) ◽  
pp. 426-429 ◽  
Author(s):  
G.-Y. Hu ◽  
Ø. Hvalby ◽  
S. I. Walaas ◽  
K. A. Albert ◽  
P. Skjeflo ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document