phorbol/hypoxia

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Delta protein kinase C interacts with the d subunit of the F1F0 ATPase in neonatal cardiac myocytes exposed to hypoxia or phorbol ester. Implications for F1F0 ATPase regulation.

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Mitochondrial protein kinase C isozymes have been reported to mediate both cardiac ischemic preconditioning and ischemia/reperfusion injury. In addition, cardiac preconditioning improves the recovery of ATP levels after ischemia/reperfusion injury. We have, therefore, evaluated protein kinase C

Phorbol ester alters rat hippocampal neuronal response to hypoxia.

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The effect of the protein kinase C (PKC) activator, 4 beta-phorbol-12, 13-dibutyrate (beta-PDBu) on electrophysiological properties of rat hippocampal CA1 neurons exposed to moderate hypoxia was examined. Hypoxic beta-PDBu-pretreated neurons differed from untreated neurons by exhibiting an

Phorbol ester alters the electrophysiological responses to hypoxia and ischemic-like conditions in the rat hippocampal slice.

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The effect of incubation with the protein kinase C activator, 4 beta-phorbol 12,13-dibutyrate (beta-PDBu) on the electrophysiological responses to hypoxia and combined hypoxia and hypoglycemia was investigated in the rat hippocampal slice. Preincubation with beta-PDBu prevents adenosine-mediated

Phorbol ester stimulates the nonhypoxic induction of a novel hypoxia-inducible factor 1alpha isoform: implications for tumor promotion.

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Hypoxia-inducible factor-1 (HIF-1), which is present at higher levels in human tumors, plays important roles in tumor promotion. It is composed of HIF-1alpha and HIF-1beta subunits and its activity depends on the amount of HIF-1alpha, which is tightly controlled by cellular oxygen tension. In

Phorbol esters stimulate muscle glucose transport by a mechanism distinct from the insulin and hypoxia pathways.

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Glucose transport in skeletal muscle can be stimulated by insulin and also by contractions and hypoxia. Activation of protein kinase C (PKC) stimulates glucose transport in muscle and other insulin-responsive cells. This study was performed to determine if the diacylglycerol (DAG)/phorbol

Ectodomain shedding of the hypoxia-induced carbonic anhydrase IX is a metalloprotease-dependent process regulated by TACE/ADAM17.

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Carbonic anhydrase IX (CA IX) is a transmembrane protein whose expression is strongly induced by hypoxia in a broad spectrum of human tumours. It is a highly active enzyme functionally involved in both pH control and cell adhesion. Its presence in tumours usually indicates poor prognosis. Ectodomain

Mapping of the vascular endothelial growth factor-producing hypoxic cells in multicellular tumor spheroids using a hypoxia-specific marker.

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We have investigated the hypoxia inducibility of vascular endothelial growth factor (VEGF) in multicellular tumor spheroids of HT29 cells using a monoclonal antibody to a fluorinated bioreductive drug, EF5 [2-(2-nitro-1H-imidazol-1-yl)-N-(2,2,3,3,3-pentafluoropropyl)aceta mide], a chemical probe for

Hypoxia switches glucose depletion-induced necrosis to phosphoinositide 3-kinase/Akt-dependent apoptosis in A549 lung adenocarcinoma cells.

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In solid tumours, necrosis is commonly found in the core region in response to metabolic stress that results from oxygen and glucose depletion (OGD) due to insufficient vascularization and has been implicated in tumour progression. We have previously shown that metabolic stress due to glucose

[Effects of hypoxia on phosphoinositide turnover and adenylate cyclase system in cultured endothelial cells].

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By studying the effects of oxygen deficiency upon signal-transducing system it has been shown that in long hypobaric hypoxia activates PI-turnover in cultured human endothelial cells. The sensitivity of cells to histamine was decreased as well as the adenylate cyclase activity in membranes of this

Involvement of protein kinase C in hypoxia-induced desensitization of the beta-adrenergic system in human endothelial cells.

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In order to better understand the mechanisms whereby oxygen deficiency promotes blunting of the endothelial beta-adrenergic receptor (beta-AR) system we examined the effects of hypoxia on beta-AR, adenylate cyclase (AC) activity and phosphoinositide turnover in cultures of human pulmonary artery and

Hypoxia-mediated impaired differentiation by LLC-PK1 cells: evidence based on the protein kinase C profile.

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We recently reported that mild hypoxia in LLC-PK1 cells, grown in standard fashion under a still layer of overlying medium at 5% CO2/18% O2 environment, result in decreased oxidative metabolism and impaired differentiated functions in comparison to adequately oxygenated cultures maintained either

Evidence that protein kinase Cepsilon mediates phorbol ester inhibition of calphostin C- and tumor necrosis factor-alpha-induced apoptosis in U937 histiocytic lymphoma cells.

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Protein kinase C (PKC) activators, such as the tumor-promoting phorbol esters, have been reported to protect several cell lines from apoptosis induced by a variety of agents. Recent evidence suggests that PKCepsilon is involved in protection of cardiac myocytes from hypoxia-induced cell death (Gray,

Hypoxia can contribute to the induction of the Epstein-Barr virus (EBV) lytic cycle.

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BACKGROUND Like other herpes viruses, latent Epstein-Barr virus (EBV) infection can be reactivated to lytic replication. Reactivation can be achieved by treatment with various reagents, including tetradecanoyl phorbol acetate (TPA) and Ca2+ ionophores. Relatively little is known about the

Chronic hypoxia augments protein kinase G-mediated Ca2+ desensitization in pulmonary vascular smooth muscle through inhibition of RhoA/Rho kinase signaling.

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Pulmonary vascular smooth muscle (VSM) sensitivity to nitric oxide (NO) is enhanced in pulmonary arteries from rats exposed to chronic hypoxia (CH) compared with controls. Furthermore, in contrast to control arteries, relaxation to NO following CH is not reliant on a decrease in VSM intracellular

Molecular mechanism of the desensitization of beta-adrenergic receptors and adenilate cyclase by hypoxia in human endothelial cells.

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Long-term oxygen deficiency in vivo leads to the progressive blunting of responsiveness to sympathetic stimulation and blood catecholamines in many human and animal tissues. In order to better understand the molecular processes that underlie this phenomenon we examined the effect of hypobaric

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