diacylglycerol/hypoxia

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Evidence for the involvement of diacylglycerol kinase in the activation of hypoxia-inducible transcription factor 1 by low oxygen tension.

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Hypoxia-inducible factor 1 (HIF-1) induces a gene expression program essential for the cellular adaptation to lowered oxygen environments. The intracellular mechanisms by which hypoxia induces HIF-1 remain poorly understood. Here we show that exposure of various cell types to hypoxia raises the

Enhanced antitumor activity of xanthohumol, a diacylglycerol acyltransferase inhibitor, under hypoxia.

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Cancer chemotherapy for hypoxic tumor cells is thought to be an important issue, since hypoxia is related to tumor growth, apoptosis, angiogenesis and metastasis. Here, the bioactivities of xanthohumol (XN), a diacylglycerol acyltransferase inhibitor, against hypoxic cells were investigated. At

Mesenchymal Stem Cells Respond to Hypoxia by Increasing Diacylglycerols.

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Mesenchymal stem cells (MSC) are currently being tested clinically for a plethora of conditions, with most approaches relying on the secretion of paracrine signals by MSC to modulate the immune system, promote wound healing, and induce angiogenesis. Hypoxia has been shown to affect MSC

Role of diacylglycerol induced by hypoxia in the regulation of HIF-1alpha activity.

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Hypoxia-inducible factor 1 (HIF-1) is a critical transcription factor for the adaptation to lowered oxygen environments. We have previously reported that hypoxia induced phosphatidic acid (PA) accumulation through diacylglycerol kinase (DGK) activity and provided evidence that this PA production

Phosphatidate, phosphatidylinositol, diacylglycerols, and free fatty acids in the brain following electroshock, anoxia, or ischemia.

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Effect of hypoxia and dopamine on arachidonic acid metabolism in superior cervical ganglion.

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Superior cervical ganglion (SCG) may play a modulatory role on ventilatory control through its efferent sympathetic fibres, which innervate cells in the carotid bodies. In this study the in vivo effect of acute hypoxia versus normoxia on arachidonic acid (AA) metabolism was investigated in cat SCG.

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

The neurotensin-HIF-1α-VEGFα axis orchestrates hypoxia, colonic inflammation, and intestinal angiogenesis.

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The expression of neurotensin (NT) and its receptor (NTR1) is up-regulated in experimental colitis and inflammatory bowel disease; NT/NTR1 interactions regulate gut inflammation. During active inflammation, metabolic shifts toward hypoxia lead to the activation of hypoxia-inducible factor (HIF)-1,

[Role of the inositol phosphate cycle in the cardioprotective effect of adaptation to intermittent hypoxia].

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The impact of adaptation to intermittent hypoxia of different duration (for 20 and 40 days) on the inositol triphosphate-diacylglycerol (ITP-DAG) regulatory contour in the heart was investigated. For this, isolated heart alpha 1-adrenoreactivity to phenylephrine and phospholipase (PhL-C) activities

Hypoxia and contractions do not utilize the same signaling mechanism in stimulating skeletal muscle glucose transport.

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We have investigated whether hypoxia and muscle contractions stimulate glucose transport in perfused rat muscle to the same extent, additively and with the same sensitivity to the microbial products calphostin C and wortmannin. Hindlimb glucose uptake increased gradually from 3.4+/-0.5 to a maximal

Inhibition effect of arachidonic acid on hypoxia-induced [Ca(2+)](i) elevation in PC12 cells and human pulmonary artery smooth muscle cells.

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[Ca(2+)](i) elevation is a key event when O(2) sensitive cells, e.g. PC12 cells and pulmonary artery smooth muscle cells, face hypoxia. Ca(2+) entry pathways in mediating hypoxia-induced [Ca(2+)](i) elevation include: voltage-gated Ca(2+) channels (VGCCs), transient receptor potential (TRP) channel

Negative regulation of diacylglycerol kinase theta mediates adenosine-dependent hepatocyte preconditioning.

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In liver ischemic preconditioning (IP), stimulation of adenosine A2a receptors (A2aR) prevents ischemia/reperfusion injury by promoting diacylglycerol-mediated activation of protein kinase C (PKC). By concerting diacylglycerol to phosphatidic acid, diacylglycerol kinases (DGKs) act as terminator of

Hypoxia training improves hepatic steatosis partly by downregulation of CB1 receptor in obese mice.

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Hypoxia training (HT) can reduce body weight and improve fatty liver. However, the mechanism is not clear. A previous study indicated that HT-induced weight loss might be associated with the endocannabinoid system (ECS), which has also been reported recently to be involved in the persistent lipid

Effects of acute hypoxia on incorporation of [1-14C]arachidonic into glycerolipids of rat brain.

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The effects of 1 min of acute hypoxic treatment (1% O2 in N2) on incorporation of [1-14C]arachidonic acid into brain lipids of 16-day-old rats were investigated at 3, 6, and 12 min after intracerebral injection of the labeled fatty acid. The hypoxic-hypoxia condition associated with convulsive

Diacylglycerol kinase (DGK) inhibitor II (R59949) could suppress retinal neovascularization and protect retinal astrocytes in an oxygen-induced retinopathy model.

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Hypoxia-inducible factors (HIF) play a fundamental role in retinal neovascularization (NV) induced by low oxygen tension. In the presence of oxygen, the HIF-α subunit becomes hydroxylated at specific prolyl residues by prolyl hydroxylases (PHD), which triggers HIF-α for degradation. In our present

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