INT58083
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Inhibition of AR prevented growth factor-induced COX-2 activity, protein, and mRNA and significantly decreased activation of nuclear factor-kappaB and protein kinase C (PKC) and phosphorylation of PKC-beta2 as well as progression of Caco-2 cell growth but had no effect on COX-1 activity. | |||||||||||||||
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Another and more relevant mechanism of long-term opioid binding is that of subsequent protein kinase C (PKC), phospholipase C (PLC) translocation and activation of nitric oxide synthetase (NOS). | |||||||||||||||
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This PLC-beta3 phosphorylation was mainly due to PKC activation because pretreatment of NG108-15 cells with calphostin C could block the DPDPE effect. | |||||||||||||||
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We recently found that repeated administration of mu-agonist causes a down regulation of mu-receptor-mediated G-protein activation, which is associated with a specific upregulation of PKC gamma isoform. | |||||||||||||||
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The effect of MENK was mediated through pertussis-toxin (PTX) sensitive G-protein and since it was abolished by H7 probably involves protein kinase C (PKC) as a second messenger system. | |||||||||||||||
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Signal transduction studies revealed that regulation of OPN was dependent on both protein kinase C (PKC) and the mitogen-activated protein (MAP) kinase cascade. | |||||||||||||||
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Tumor-promoting phorbol esters activate protein kinase C (PKC) isozymes by binding to the zinc-finger like cysteine-rich domains in the N-terminal regulatory region. | |||||||||||||||
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Regulation by protein phosphorylation was suggested by the observations that the opioid-mediated response was potentiated by calphostin C, an inhibitor of protein kinase C (PKC), and was abolished by either phorbol-12-myristate-13-acetate, a PKC activator, or calyculin A, a protein phosphatase1/2A inhibitor. | |||||||||||||||
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The stability of PKC zeta and PKM zeta in SD indicates that a molecular mechanism for the maintenance of LTP/ LTD is relatively resistant to alterations that occur during pathophysiologically large ionic fluxes. | |||||||||||||||
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Opioid receptor stimulation induced a calcium-dependent protein kinase C alpha (PKC alpha)/extracellular regulated kinase (ERK)/phosphatidylinositol 3-kinase (PI3K) pathway activation that mediated the effect of endogenous opioids on HSC proliferation and collagen synthesis. | |||||||||||||||
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MENK induced O2- release was associated with a dose-dependent increase of diacylglycerol (DAG) concentration and protein-kinase C (PKC) translocation to the neutrophil membranes, with an increase of cytosolic Ca++, and could be abolished by H7, a PKC inhibitor. | |||||||||||||||
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General Comments
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