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Gene target: hexokinase 3


Symbol : Hexokinase NIH gene
chromosome : Un
description : hexokinase type 2
type of gene : protein-coding
Modification date : 2015-11-14

Related Pathways to: MOUSE ANTI RAT HEXOKINASE 3

Gene about :Hexokinase
Pathway :Hs Cori Cycle

Related product to: MOUSE ANTI RAT HEXOKINASE 3

Related Articles about: MOUSE ANTI RAT HEXOKINASE 3

Acute detachment of hexokinase II from mitochondria modestly increases oxygen consumption of the intact mouse heart.

Cardiac hexokinase II (HKII) can translocate between cytosol and mitochondria and change its cellular expression with pathologies such as ischemia-reperfusion, diabetes and heart failure. The cardiac metabolic consequences of these changes are unknown. Here we measured energy substrate utilization in cytosol and mitochondria using stabile isotopes and oxygen consumption of the intact perfused heart for 1) an acute decrease in mitochondrial HKII (mtHKII), and 2) a chronic decrease in total cellular HKII. - Source :PubMed

Succinate-induced neuronal mitochondrial fission and hexokinase II malfunction in ischemic stroke: Therapeutical effects of kaempferol.

Mitochondrial dysfunction is known as one of causative factors in ischemic stroke, leading to neuronal cell death. The present work was undertaken to investigate whether succinate induces neuron apoptosis by regulating mitochondrial morphology and function. In neurons, oxygen-glucose deprivation induced succinate accumulation due to the reversal of succinate dehydrogenase (SDH) activation, leading to mitochondrial fission. Kaempferol inhibited mitochondrial fission and maintained mitochondrial HK-II through activation of Akt, and thereby protected neurons from succinate-mediated ischemi injury. Knockdown of Akt2 with siRNA diminished the effect of kaempferol, indicating that kaempferol suppressed dynamin-related protein 1 (Drp1) activation and promoted HK-II mitochondrial binding dependently on Akt. Moreover, we demonstrated that kaempferol potentiated autophagy during oxygen and glucose deprivation, contributing to protecting neuron survival against succinate insult. In vivo, oral administration of kaempferol in mice attenuated the infract volume after ischemic and reperfusion (I/R) injury and reproduced the similar mitochondrial protective effect in the brain infract area. This study indicates that succinate accumulation plays a pivotal role in I/R injury-induced neuronal mitochondrial dysfunction, and suggests that modulation of Drp1 phosphorylation might be potential therapeutic strategy to protect neuron mitochondrial integrity and treat ischemic stroke. - Source :PubMed

Molecular Cloning and Functional Characterization of a Hexokinase from the Oriental River Prawn Macrobrachium nipponense in Response to Hypoxia.

Metabolic adjustment to hypoxia in Macrobrachium nipponense (oriental river prawn) implies a shift to anaerobic metabolism. Hexokinase (HK) is a key glycolytic enzyme in prawns. The involvement of HK in the hypoxia inducible factors (HIFs) pathway is unclear in prawns. In this study, the full-length cDNA for HK (MnHK) was obtained from M. nipponense, and its properties were characterized. The full-length cDNA (2385 bp) with an open reading frame of 1350 bp, encoded a 450-amino acid protein. MnHK contained highly conserved amino acids in the glucose, glucose-6-phosphate, ATP, and Mg(+2) binding sites. Quantitative real-time reverse transcription PCR assays revealed the tissue-specific expression pattern of MnHK, with abundant expression in the muscle, and gills. Kinetic studies validated the hexokinase activity of recombinant HK. Silencing of HIF-1α or HIF-1β subunit genes blocked the induction of HK and its enzyme activities during hypoxia in muscles. The results suggested that MnHK is a key factor that increases the anaerobic rate, and is probably involved in the HIF-1 pathway related to highly active metabolism during hypoxia. - Source :PubMed

Conformational Characteristics of Rice Hexokinase OsHXK7 as a Moonlighting Protein involved in Sugar Signalling and Metabolism.

Hexokinase (HXK) as a moonlighting protein involves in glucose metabolism and signalling to regulate growth and development in plants. Therefore, the clarification for the structural properties of OsHXK7 (Oryza sativa Hexokinase 7) is essential to understand its role mechanism associated with the Glc signalling and metabolism. In this study, the structural characteristics of OsHXK7 (Oryza sativa Hexokinase 7) were identified. In the fluorescence spectrum, the Trp peak representing OsHXK7 binding to D-glucose (D-Glc) and 2-deoxyglucose (2-dG) showed an obvious blue shift. The distinct change in the secondary structure of OsHXK7 after binding to Glc was also detected in circular dichroism spectra. Using superimposed modelling, OsHXK7 showed a Glc-induced structural change, in which the 76th glycine, 148th serine and 256th tryptophan were contained within the pocket region. It was further shown by site-directed mutagenesis that the 76th glycine and the 256th tryptophan, but not the 148th serine, are the pivotal sites of OsHXK7 that maintain its catalytic activity and intrinsic blue shift fluorescence. These results suggest that OsHXK7 binding to Glc leads to a conformational change, that is likely essential for the function of OsHXK7 in Glc signalling and metabolism during plant growth and development. - Source :PubMed

Inhibition of miR-143 during ischemia cerebral injury protects neurons through recovery of the Hexokinase 2-mediated glucose uptake.

Ischemic stroke, a major cause of death, is caused by occlusion of a blood vessel, resulting in a significant reduction in regional cerebral blood flow. MicroRNAs (miRNAs) are a family of short noncoding RNAs (18 to 22 nucleotides) and bind the 3' un-translated region (UTR) of their target genes to post-transcriptionally suppress gene expression. In this study, we report miR-143 is downregulated in rat neurons but high expressed in astrocytes cells. In vivo middle cerebral artery occlusion (MCAO) and ex vivo oxygen-glucose deprivation (OGD) results showed miR-143 was significantly induced by ischemia injury. Meanwhile, we observed suppression of glucose uptake and lactate product of rat brain and primary neurons after MCAO or OGD. The glycolysis enzymes Hexokinase 2 (HK2), PKM2 and LDHA were inhibited by MCAO or OGD at protein and mRNA levels. In addition, overexpression of miR-143 significantly inhibited HK2 expression and glucose uptake and lactate product. We report HK2 is a direct target of miR-143. Importantly, restoration of HK2 in miR-143 overexpressing rat neurons recovered glucose uptake and lactate product. Our results demonstrated inhibition of miR-143 during OGD could protect rat neuronal cells from ischemia brain injury. In summary, this study reveals a miRNAs-mediated neuron protection during ischemic brain injury (IBI), providing a new strategy for the development of therapeutic agents against ischemia brain injury. - Source :PubMed

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