3 beta galactosidase/hypoxia

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Effect of hypoxia duration on the oxygen-dependent production of a recombinant protein, β-galactosidase, by an animal cell line, F6D2, with a hypoxia-inducible enhancer.

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Expression of specific genes is a strategy of animal cells for adaptation to oxygen deficiency and the mechanism underlying the hypoxic activation of gene expression may be useful for efficient production of recombinant proteins by animal cells, because oxygen is a limiting factor in animal cell

Hypoxia-inducible factor 1 activation from adipose protein 2-cre mediated knockout of von Hippel-Lindau gene leads to embryonic lethality.

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von Hippel-Lindau protein, an E3 ubiquitin ligase from the von Hippel-Lindau (Vhl) gene, inhibits the transcriptional activity of hypoxia-inducible factor 1α in cells. To gain insight into the hypoxia-inducible factor 1α signalling pathway in adipose tissue, a study was conducted to generate

Generation of bidirectional hypoxia/HIF-responsive expression vectors to target gene expression to hypoxic cells.

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Hypoxia initiates an adaptive physiological response in all organisms and plays a role in the pathogenesis of several human diseases. The hypoxia/HIF-inducible factor-1 (HIF-1) transcription factor mediates transcriptional responses to hypoxia by binding to a cis-acting hypoxia-responsive element

A novel method for targeted gene therapy in ischemic tissues through viral transfection of an expression cassette containing multiple repetitions of hypoxia response element.

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BACKGROUND Increased levels of the transcription factor hypoxia inducible factor (HIF)-1 occur only in hypoxic tissue. The authors propose a therapeutic strategy that relies on HIF-1, the enhancer hypoxia response element (HRE), and the delivery vector adeno-associated virus-2 (AAV2) to direct

Stimuli that induce a yeast heat shock gene fused to beta-galactosidase.

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Saccharomyces cerevisiae contain a multigene family related to the Drosophila heat shock gene hsp70. Two members of this family, YG100 and YG101, have been previously characterized (Ingolia et al., Mol. Cell. Biol. 2:1388-1398, 1982), and only YG100 was found to have elevated levels of transcription

Hypoxia reoxygenation induces premature senescence in neonatal SD rat cardiomyocytes.

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OBJECTIVE To investigate whether hypoxia reoxygenation induces premature senescence in neonatal Sprague-Dawley (SD) rat cardiomyocytes. METHODS Cardiomyocytes were isolated from neonatal SD rat heart and identified by immunohistochemistry. The control cultures were incubated at 37 degree centigrade

Up-regulation of vascular endothelial growth factor expression in a rat glioma is conferred by two distinct hypoxia-driven mechanisms.

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Up-regulation of vascular endothelial growth factor (VEGF) expression is a major event leading to neovascularization in malignant gliomas. Hypoxia is believed to be the crucial environmental stimulus for this up-regulation. To critically assess this hypothesis, we asked whether the mechanisms

p21 WAF1 and hypoxia/reoxygenation-induced premature senescence of H9c2 cardiomyocytes.

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We have previously reported on hypoxia/reoxygenation-induced premature senescence in neonatal rat cardiomyocytes. In this research, we investigated the effects of p21(WAF1) (p21) in hypoxia/reoxygenation-induced senescence, using H9c2 cells. A plasmid overexpressing wild type p21(WAF1) and a plasmid

Hypoxia-reoxygenation induces premature senescence in FA bone marrow hematopoietic cells.

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Hematopoietic cells are often exposed to transient hypoxia and reoxygenation as they develop and migrate. Given that bone marrow (BM) failure occurred in patients with Fanconi anemia (FA), we reason that hypoxia-then-reoxygenation represents a physiologically relevant stress for FA hematopoietic

[Effects of hypoxia on endothelial nitric oxide synthase gene expression in pulmonary artery endothelial cells and the role of protein kinase C isoforms].

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OBJECTIVE To explore the regulation of eNOS gene expression in pulmonary arterial endothelial cells (PAECs) by protein kinase C (PKC) and its isoforms during hypoxia. METHODS Primary cultured porcine PAECs were exposed to 5%O(2) for 2, 6, 12, 24, 48 hours. The eNOS mRNA level was measured by RT-PCR.

Silencing thioredoxin induces liver cancer cell senescence under hypoxia.

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OBJECTIVE Although thioredoxin 1 (TXN) has pleiotropic cellular functions as a redox-sensitive protein, very little is known about its role in tumor survival and growth under hypoxia. MHCC97H hepatocellular carcinoma cells have a high metastatic potential and high thioredoxin expression levels

Oxygen sensitivity of reporter genes: implications for preclinical imaging of tumor hypoxia.

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Reporter gene techniques have been applied toward studying the physiologic phenomena associated with tumor hypoxia, a negative prognostic indicator. The purpose of this study was to assess the potential adverse effects of hypoxic conditions on the effectiveness of four commonly used reporter genes:

A nuclear localization signal of human aryl hydrocarbon receptor nuclear translocator/hypoxia-inducible factor 1beta is a novel bipartite type recognized by the two components of nuclear pore-targeting complex.

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Aryl hydrocarbon receptor nuclear translocator (ARNT) is a component of the transcription factors, aryl hydrocarbon receptor (AhR) and hypoxia-inducible factor 1, which transactivate their target genes, such as CYP1A1 and erythropoietin, in response to xenobiotic aromatic hydrocarbons and to low O2

Biological time-related changes in tolerance of male mice to hypoxia--II. Circadian rhythm of lysosomal susceptibility to hypoxia.

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Circadian variations of mouse liver, brain and heart lysosomal susceptibility to hypoxia were investigated. Lysosomal disruption during hypoxia was estimated on the basis of the following measurements: changes in percentage free activity of beta-galactosidase and acid phosphatase, tissue loss of

Recombinant gene transfer of endothelial nitric oxide synthase augments coronary artery relaxations during hypoxia.

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BACKGROUND Coronary arteries respond to hypoxia with transient relaxations, which increases coronary blood flow, in part, by release of nitric oxide. We hypothesized that increased expression of nitric oxide synthase might further augment blood vessel relaxation during hypoxia. The present study

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