Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.11.13 (protein kinase C)
 49,245 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Heparin-binding growth factors (HBGF) are essential and key mitogens for human adult large vessel endothelial cells. At 170 pg/ml, the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) caused a 50% inhibition of heparin-binding growth factor type one (HBGF-1)-stimulated DNA synthesis in human adult large vessel endothelial cells. TPA at 1 ng/ml completely inhibited HBGF-1-stimulated proliferation. TPA at 5 ng/ml reduced specific HBGF-1 receptor sites from 6600 per cell to 3200 per cell without affecting receptor affinity. Since phorbol esters are potent activators of protein kinase C, desensitizes both animal capillary and human adult large vessel endothelial cells to the mitogenic effects of HBGF by down-regulation of specific HBGF receptors.--HOSHI, H; KAN, M.; MIOH, H.; CHEN J.-K.; McKEEHAN, W. L. Phorbol ester reduces number of heparin-binding growth factor receptors in human adult endothelial cells.
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PMID:Phorbol ester reduces number of heparin-binding growth-factor receptors in human adult endothelial cells. 245 32

Neuropeptide Y (NPY) attenuated angiotensin II (AII)-or bradykinin (BK)-induced Ca2+ release from intracellular stores and inhibited forskolin-stimulated cAMP accumulation and omega-conotoxin-sensitive high K(+)-induced Ca2+ influx in the human neuroblastoma cell line SMS-KAN. All three NPY actions were mediated via Y2 receptors. Pretreatment with pertussis toxin completely abolished all of the NPY actions. Activation or down-regulation of protein kinase C had no effect on any NPY-mediated effect; herbimycin A, a tyrosine kinase inhibitor, only abolished the inhibitory effect of NPY on AII- or BK-induced Ca2+ mobilization. Herbimycin A also blocked platelet-derived growth factor-induced Ca2+ mobilization, which involves tyrosine kinase activation, and there was a good correlation in the concentration dependency between the two effects of herbimycin A, strongly suggesting that its ability to cancel the NPY effect is due to inhibition of tyrosine kinase activity. NPY attenuated AII- or BK-induced inositol 1,4,5-trisphosphate production, and herbimycin A reversed this NPY effect. These results provide the first evidence that Y2 receptors negatively couple to AII- or BK-induced phosphoinositide turnover leading to Ca2+ mobilization through pertussis toxin-sensitive GTP-binding protein(s). Inhibition of phospholipase C-beta activity by NPY seems to be mediated by activation of protein-tyrosine kinase or phosphotyrosine-containing protein(s).
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PMID:Y2 receptors for neuropeptide Y are coupled to three intracellular signal transduction pathways in a human neuroblastoma cell line. 813 19