Staurosporine inhibits cell proliferation and in vivo protein phosphorylation induced by phorbolester.
2
The C2 domain-swapped mutants were inactive in phorbolester-induced membrane translocation.
3
Such an effect was not seen with inactive phorbolester.
4
In contrast, basal and phorbolester-stimulated PLD activities were not or only slightly reduced.
5
In the presence of cholesterol sulfate, phorbolester only weakly enhanced the activity of nPKC eta.
6
These samples were stimulated ex vivo with phorbolester and were assayed for PKC activity using this approach.
7
Plating onto basement membrane matrix and stimulation by phorbolester were used as in vitro models of angiogenesis.
8
Inhibition of Fas-mediated cell death by phorbolester is also observed in other human leukemic T cell lines.
9
We conclude that the iridals represent a promising structural motif for design of ligands for phorbolester receptor family members.
10
Functional studies implicate AP1-1 and AP1-5 in mediating the phorbolester-dependent increase in promoter activity.
11
Involucrin mRNA levels increase 10-fold and promoter activity 5-11-fold when differentiation is induced by phorbolester.
12
In this report, we show that all these effects are substantially inhibited by the activation of PKC with a phorbolester.
13
CD45 redistribution does not require hydrolysis of phosphatidylinositides and cannot be reproduced by the addition of phorbolester and calcium ionophore.
14
Raising of intracellular cGMP by 8-bromo-cGMP and activation of protein kinase C by phorbolester led to an inhibition of secretion.
15
An important prediction of this hypothesis is that inhibitors of PKC should inhibit these phorbolester-induced changes in bag cell neuronal excitability.
16
Activation of PKC using phorbolester resulted in an increase of adhesive interactions under dynamic and static conditions, whereas its inhibition reduced adhesion.