sterol/hypoxia

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Stra13/DEC1 and DEC2 inhibit sterol regulatory element binding protein-1c in a hypoxia-inducible factor-dependent mechanism.

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Sterol regulatory element binding protein-1c (SREBP-1c) is a basic helix-loop-helix (bHLH) homodimeric transactivator, which induces itself and several lipogenic enzymes, notably fatty acid synthase (FAS). We demonstrated that hypoxia-inducible factor (HIF) represses the SREBP-1c gene by inducing

FoxO4 interacts with the sterol regulatory factor SREBP2 and the hypoxia inducible factor HIF2α at the CYP51 promoter.

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The late steps of cholesterol biosynthesis are oxygen demanding, requiring eleven oxygen molecules per synthesized cholesterol molecule. A key enzymatic reaction, which occurs at the top of the Bloch and Kandutsch-Russell pathways, is the demethylation of lanosterol and dihydrolanosterol (DHL). This

Free sterols of the cerebral white matter in experimental severe hypoxia.

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Wistar rats, aged 3.5 months, were subjected to severe hypoxia by placing them for 3 minutes in an atmosphere containing 2 kPa of oxygen. The myelin fraction was isolated from brains of the experimental animals at the following periods after the hypoxia event: 4 and 24 hours, 14 days, 2 months. The

The effect of moderate hypoxia on free sterols: content and pattern in white matter.

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Wistar rats underwent moderate hypoxia by exposing them to a respiratory gas mixture containing 7% oxygen, for 30 min. The myelin was analyzed at 4 h 24 h, day 14, and day 60 after hypoxia. The group of neutral lipids isolated from myelin was analyzed by GC-MS (gas chromatography-mass spectrometry)

Patterns of free and esterified sterol fractions of the cerebral white matter in severe and moderate experimental hypoxia.

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Cerebral sterols were examined in Wistar strain rats, subjected 4 h, 24 h, 14 days or 2 months earlier to severe (2% oxygen) and moderate (7% oxygen) experimental hypoxia. From brains of the experimental animals myelin was isolated and examined by gas chromatography coupled with mass spectrometry

Effects of hypoxia on sterol synthesis, acyl-CoA:cholesterol acyltransferase activity, and efflux of cholesterol in cultured rabbit skin fibroblasts.

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To elucidate the mechanisms of cholesterol accumulation in cells under hypoxic conditions, we tested the effects of hypoxia on sterol synthesis, on the activity of acyl-CoA:cholesterol acyltransferase (ACAT), and on the efflux of cholesterol in cultured rabbit skin fibroblasts. Sterol synthesis was

Transcriptional downregulation of sterol metabolism genes in murine liver exposed to acute hypobaric hypoxia.

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Ascent to high-altitude results in decreased inspired partial pressure of oxygen because of a decrease in barometric pressure. Altitude acclimatization requires physiological and metabolic changes to improve tolerance to altitude hypoxia. Cellular response to hypoxia results into changes in the

Composition of the cerebral white matter sterol ester fraction in severe experimental hypoxia.

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Severe hypoxia was induced in adult Wistar rats by means of exposure to an atmosphere containing 2.0 kPa of oxygen for a period of 3 minutes. The animals were sacrificed at 4 different periods following the hypoxia incident: 4 and 24 hours, 14 days and 2 months, respectively, and sterol esters (ES)

Ganoderma total sterol (GS) and GS1 protect rat cerebral cortical neurons from hypoxia/reoxygenation injury.

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The effect of Ganoderma total sterol (GS) and its main components(GS(1)) on rat cortical neuronal cultures exposed to hypoxia/reoxygenation (H/R) was studied in vitro. GS (0.01,0.1,1 microg/ml) increased neuron viability following H/R. GS also significantly reduced malondialdehyde content and

Cobalt chloride, a hypoxia-mimicking agent, targets sterol synthesis in the pathogenic fungus Cryptococcus neoformans.

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We investigated the effects of the hypoxia-mimetic CoCl2 in the pathogenic fungus Cryptococcus neoformans and demonstrated that CoCl2 leads to defects in several enzymatic steps in ergosterol biosynthesis. Sterol defects were amplified in cells lacking components of the Sre1p-mediated oxygen-sensing

A sterol-regulatory element binding protein is required for cell polarity, hypoxia adaptation, azole drug resistance, and virulence in Aspergillus fumigatus.

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At the site of microbial infections, the significant influx of immune effector cells and the necrosis of tissue by the invading pathogen generate hypoxic microenvironments in which both the pathogen and host cells must survive. Currently, whether hypoxia adaptation is an important virulence

Fatty acid synthase gene is up-regulated by hypoxia via activation of Akt and sterol regulatory element binding protein-1.

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The fatty acid synthase (FAS) gene is significantly up-regulated in various types of cancers, and blocking the FAS expression results in apoptosis of tumor cells. Therefore, FAS is considered to be an attractive target for anticancer therapy. However, the molecular mechanism by which the FAS gene is

The signal peptide peptidase SppA is involved in sterol regulatory element-binding protein cleavage and hypoxia adaptation in Aspergillus nidulans.

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Using forward genetics, we revealed that the signal peptide peptidase (SPP) SppA, an aspartyl protease involved in regulated intramembrane proteolysis (RIP), is essential for hypoxia adaptation in Aspergillus nidulans, as well as hypoxia-sensitive mutant alleles of a sterol regulatory

The fungal mitochondrial membrane protein, BbOhmm, antagonistically controls hypoxia tolerance.

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Adaptation to low-oxygen environment in host tissues is crucial for microbial pathogens, particuarlly fungi, to successfully infect target hosts. However, the underlying mechanisms responsible for hypoxia tolerance in most pathogens are poorly understood. A mitochondrial protein, BbOhmm, is

AMPKα Subunit Ssp2 and Glycogen Synthase Kinases Gsk3/Gsk31 are involved in regulation of sterol regulatory element-binding protein (SREBP) activity in fission yeast.

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Sterol regulatory element-binding protein (SREBP), a highly conserved family of membrane-bound transcription factors, is an essential regulator for cellular cholesterol and lipid homeostasis in mammalian cells. Sre1, the homolog of SREBP in the fission yeast Schizosaccharomyces pombe (S. pombe),

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