aminopurine/hypoxia

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Gadd45 and Gadd153 messenger RNA levels are increased during hypoxia and after exposure of cells to agents which elevate the levels of the glucose-regulated proteins.

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We have investigated overlapping activation pathways for two families of stress genes that are expressed in cells exposed to hypoxia. The growth arrest and DNA damage (gadd) genes are induced by DNA damage and irradiation, and their expression is associated with growth arrest. The glucose-regulated

Reactive oxygen species production by mitochondria in endothelial cells exposed to reoxygenation after hypoxia and glucose depletion is mediated by ceramide.

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In endothelium, reoxygenation after hypoxia (H/R) has been shown to induce production of reactive oxygen species (ROS) by complex III of the mitochondrial respiratory chain. The purpose of the present study was to test the involvement of ceramide in this phenomenon. Human umbilical vein endothelial

Effect of protein kinase and phosphatase inhibitors on expression of hypoxia-inducible factor 1.

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Hypoxia-inducible factor 1 (HIF-1) is a heterodimeric bHLH-PAS protein essential for erythropoietin gene transcription in hypoxic cells. Here we show that both 2-aminopurine and sodium fluoride, inhibitors of serine/threonine kinases and phosphatases, respectively, interfered with the hypoxic

Characterization of hypoxia-inducible factor 1 and regulation of DNA binding activity by hypoxia.

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Hypoxia-inducible factor 1 (HIF-1) is a DNA binding activity detected in nuclear extracts from Hep3B cells cultured in 1% O2 but not in extracts from cells cultured in 20% O2. HIF-1 binds to a sequence within the human erythropoietin gene enhancer that is required for hypoxic activation of

NGF protects PC12 cells against ischemia by a mechanism that requires the N-kinase.

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Nerve growth factor (NGF), which has been shown to act as a morphological and neurochemical differentiating factor in PC12 cells, also protects PC12 cells from the toxicity of serum withdrawal and ischemia. By using a previously established in vitro model of ischemia, which incorporates the

Inhibitors and pathways of hepatocytic protein degradation.

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On the basis of experiments using amino acids and various inhibitors (lysosomotropic amines, leupeptin, chymostatin, vanadate, vinblastine, anoxia, methylaminopurines), five different modes of endogenous protein degradation in isolated rat hepatocytes can be distinguished. The two non-lysosomal

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