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glutamate dehydrogenase/hypoxia
Link salvestatakse lõikelauale
Leht 1 alates 60 tulemused
An enzymatic bridge between carbohydrate and amino acid metabolism: regulation of glutamate dehydrogenase by reversible phosphorylation in a severe hypoxia-tolerant crayfish.
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Glutamate dehydrogenase (GDH) (EC 1.4.1.3) is a crucial enzyme involved in bridging two metabolic pathways, gating the use of glutamate for either amino acid metabolism, or carbohydrate metabolism. The present study investigated GDH from tail muscle of the freshwater crayfish Orconectes virilis
miR‑30a‑5p inhibits hypoxia/reoxygenation‑induced oxidative stress and apoptosis in HK‑2 renal tubular epithelial cells by targeting glutamate dehydrogenase 1 (GLUD1)
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MicroRNAs (miRNAs) are reported to be involved in renal hypoxia/reoxygenation (H/R) damage. To investigate this further, human kidney (HK‑2) cells were cultured, subjected to H/R and the function of miR‑30a‑5p and glutamate dehydrogenase 1 (GLUD1) was evaluated. The results showed that, miR‑30‑5p
Ethylene-Regulated Glutamate Dehydrogenase Fine-Tunes Metabolism during Anoxia-Reoxygenation.
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Ethylene is an essential hormone in plants that is involved in low-oxygen and reoxygenation responses. As a key transcription factor in ethylene signaling, ETHYLENE INSENSITIVE3 (EIN3) activates targets that trigger various responses. However, most of these targets are still poorly characterized.
Reconfiguration of N Metabolism upon Hypoxia Stress and Recovery: Roles of Alanine Aminotransferase (AlaAT) and Glutamate Dehydrogenase (GDH).
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In the context of climatic change, more heavy precipitation and more frequent flooding and waterlogging events threaten the productivity of arable farmland. Furthermore, crops were not selected to cope with flooding- and waterlogging-induced oxygen limitation. In general, low oxygen stress, unlike
Rg1 prevents myocardial hypoxia/reoxygenation injury by regulating mitochondrial dynamics imbalance via modulation of glutamate dehydrogenase and mitofusin 2.
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OBJECTIVE
Mitochondrial dysfunction is a prominent feature of ischemia heart disease but the underlying mechanism of dynamics (fusion/fission) is still unclear. Here we investigated a novel function and underlying mechanism of Rg1 on an in vitro cardiomyocyte model of hypoxia/reoxygenation
[Effect of anoxia on the oxidative phosphorylation processes and on glutamate dehydrogenase activity in the central nervous system].
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[Clinical significance of the glutamate dehydrogenase activity in serum with special reference to liver damage induced by hypoxia].
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[Histochemical picture of lactate dehydrogenase, succinic dehydrogenase and glutamate dehydrogenase in the central nervous system of rats exposed repeatedly for a prolonge period to aerogenic hypoxia during early ontogenesis (author's transl)].
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[Effect of glutamic acid on the activity of glutamate dehydrogenase, Mg 2+ -and dinitrophenol-stimulating adenosine triphosphatases in rat kidney, heart and liver mitochondria during acute and chronic hypoxia].
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Effects of fructose-1,6-bisphosphate on glutamate release and ATP loss from rat brain slices during hypoxia.
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Fructose-1,6-bisphosphate (FBP), an intermediate of glucose metabolism, is neuroprotective in brain hypoxia or ischemia. Because the mechanisms for this protection are not clear, we examined the effects of FBP on two important events in brain ischemia, i.e., loss of ATP and release of the excitatory
Visualization of hypoxia-induced glutamate release in gerbil hippocampal slice.
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Microfluorometry was used to investigate distribution of hypoxia-induced release of glutamate. Mongolian gerbil hippocampal slice was perfused in a medium containing glutamate dehydrogenase and NAD+. Release of glutamate into extracellular space caused an increase in fluorescence due to the
Failure of glutamate dehydrogenase system to predict oxygenation state of human skeletal muscle.
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In a recent study, the total tissue contents of glutamate (Glu), ammonium (NH+4), and 2-oxoglutarate (2-OG) were used to estimate changes in the mitochondrial redox state ([NAD+]/[NADH]) of contracting skeletal muscle with intact circulation [Am. J. Physiol. 253 (Cell Physiol. 22): C263-C268, 1987].
Volatile and intravenous anesthetics decrease glutamate release from cortical brain slices during anoxia.
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BACKGROUND
Extracellular accumulation of the excitatory neurotransmitter L-glutamate during cerebral hypoxia or ischemia contributes to neuronal death. Anesthetics inhibit release of synaptic neurotransmitters but it is unknown if they alter net extrasynaptic glutamate release, which accounts for
[Effects of exogenous NO3- on cherry root function and enzyme activities related to nitrogen metabolism under hypoxia stress].
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A water culture experiment with controlled dissolved oxygen concentration was conducted to explore the effects of exogenous NO3- on the root function and enzyme activities related to nitrogen metabolism of cherry (Prunun cerasus x P. canescens) seedlings under hypoxia stress. Comparing with the
Effect of hypoxia, aging and pharmacological treatment on muscular metabolites and enzyme activities.
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The effect of hypoxia and post-hypoxic recovery were studied in gastrocnemius muscle of young-adult and mature beagle dogs. Furthermore, the possible interference of pharmacological treatment with nicergoline was evaluated in these conditions. Muscular glycolytic fuels, intermediates and
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