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235 results for “glycolysis”
Pyruvate transamination and NAD biosynthesis enable proliferation of succinate dehydrogenase-deficient cells by supporting aerobic glycolysis
<p>Data supporting results published by Ricci et al. Pyruvate transamination and NAD biosynthesis enable proliferation of succinate dehydrogenase-deficient cells by supporting aerobic glycolysis. Cell Death and Disease (2023) 14:403 (https://doi.org/10.1038/s41419-023-05927-5).</p>
Supporting information for prebiotic triose glycolysis promoted by co-catalytic proline and phosphate in neutral water
<p>Supporting information for prebiotic triose glycolysis promoted by co-catalytic proline and phosphate in neutral water</p>
The reaction mechanism for glycolysis side product degradation by Parkinson's disease-linked DJ-1
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Human airway macrophages are metabolically reprogrammed by IFN-γ resulting in glycolysis-dependent functional plasticity
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Data from: TIPE drives a cancer stem-like phenotype by promoting glycolysis via PKM2/HIF-1α axis in melanoma
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Dexamethasone inhibits Mycobacterium tuberculosis-induced glycolysis but preserves antimicrobial function in primary human macrophages.
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Properties of recovered polyols by glycolysis of polyurethane waste foams
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Dataset related to: Post-translational modifications by SIRT3 de-2-hydroxyisobutyrylase activity regulate glycolysis and enable nephrogenesis
<p>The file contains all the dataset included in the manuscript, divided by figure in each tab</p> <p> </p> <p><strong>Abstract</strong></p> <p>Abnormal kidney development leads to lower nephron number, predisposing to renal diseases in adulthood. In embryonic kidneys, nephron endowment is dictated by the availability of nephron progenitors, whose self-renewal and differentiation require a relatively repressed chromatin state. More recently, NAD<sup>+</sup>-dependent deacetylase sirtuins (SIRTs) have emerged as possible regulators that link epigenetic processes to the metabolism. Here, we discovered a novel role for the NAD<sup>+</sup>-dependent deacylase SIRT3 in kidney development. In the embryonic kidney, SIRT3 was highly expressed only as a short isoform, with nuclear and extra-nuclear localisation. The nuclear SIRT3 did not act as deacetylase but exerted de-2-hydroxyisobutyrylase activity on lysine residues of histone proteins. Extra-nuclear SIRT3 regulated lysine 2-hydroxyisobutyrylation (Khib) levels of phosphofructokinase (PFK) and Sirt3 deficiency increased PFK Khib levels, inducing a glycolysis boost. This altered Khib landscape in <em>Sirt3<sup>-/-</sup></em> metanephroi was associated with decreased nephron progenitors, impaired nephrogenesis and a reduced number of nephrons. These data describe an unprecedented role of SIRT3 in controlling early renal development through the regulation of epigenetics and metabolic processes.</p>
miR-1285-3p targets TPI1 to regulate the glycolysis metabolism signaling pathway of Tibetan sheep Sertoli cells
<p><span>Glycolysis in sertoli cells (SCs) can provide energy substrates for the development of spermatogenic cells. Triose phosphate isomerase 1 (TPI1) is one of the key catalytic enzymes involved in glycolysis. However, the biological function of TPI1 in SCs and its role in glycolytic metabolic pathways are poorly understood. On the basis of previous research, we isolated primary SCs from Tibetan sheep and overexpressed <em>TPI1</em> gene to determine its effect on the proliferation, glycolysis, and apoptosis of SCs. Secondly, we investigated the relationship between <em>TPI1</em> and miR-1285-3p, and whether miR-1285-3p regulates the proliferation and apoptosis of SCs, and participates in glycolysis by targeting <em>TPI1</em>. Results showed that overexpression of <em>TPI1</em> increased the proliferation rate and decreased apoptosis of SCs. In addition, overexpression of <em>TPI1</em> altered glycolysis and metabolism signaling pathways and significantly increased the amount of the final product lactic acid. Further analysis showed that miR-1285-3p inhibited <em>TPI1</em> by directly targeting its 3'untranslated region. Overexpression of miR-1285-3p suppressed the proliferation of SCs, and this effect was partially reversed by restoration of <em>TPI1</em> expression. In summary, this study shows that the miR-1285-3p/TPI1 axis regulates glycolysis in SCs. These findings add to our understanding of the regulation of spermatogenesis in sheep and other mammals.</span></p>
Enhancing cardiac glycolysis causes an increase in PDK4 content in response to short term high fat diet
<p>Cardiac metabolic flexibility is essential for proper function. Under pathological conditions, such as diabetes, the heart increases reliance on fatty acid oxidation at the expense of glucose metabolism. Thus, restoring or enhancing glucose usage may provide a therapeutic strategy. In this study we sought to identify how the cardiac proteomic profile is affected basally and after a short term high fat diet (7d) in wild type and a transgenic model of enhanced glycolysis (Glyco<sup>Hi</sup>). Targeted quantitative proteomics and cluster analysis revealed revealed Glyco<sup>Hi</sup> mice have increased protein expression of glycolytic enzymes and that this was sustained with the high fat diet challenge. Glyco<sup>Hi</sup> mice also had significantly increased expression of pyruvate dehydrogenase kinase 4 (PDK4), an enzyme that regulates the overall rate of glucose oxidation. These results support that Glyco<sup>Hi</sup> mice have the capacity to increase glycolysis when challenged with a nutrient stress but that there is a compensatory increase in PDK4 that may limit the overall rate of glucose oxidation.</p>
GSK-3ß inhibitor and Actinonin can eliminate HNF-1ß overexpression in Clear Cell Carcinoma through glycolysis inhibition and mitochondrial turnover.
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Is Dietary Nitrate Effective in Reducing Aerobic Glycolysis in Breast Cancer?
ClinicalTrials.gov study NCT03944226. IPD Sharing: NO. Countries: 1. Publications: 6.
Metabolic Inflexibility is Related to Elevated Muscle Anaerobic Glycolysis
ClinicalTrials.gov study NCT04320264. IPD Sharing: NO. Countries: 1. Publications: 5.
miR-1285-3p targets TPI1 to regulate the glycolysis metabolism signaling pathway of Tibetan sheep Sertoli cells
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Data from: Acute maneb exposure significantly alters both glycolysis and mitochondrial function in neuroblastoma cells
The pesticides paraquat (PQ) and maneb (MB) have been described as environmental risk factors for Parkinson's disease (PD), with mechanisms associated with mitochondrial dysfunction and reactive oxygen species generation. A combined exposure of PQ and MB in murine models and neuroblastoma cells has been utilized to further advance understanding of the PD phenotype. MB acts as a redox modulator through alkylation of protein thiols and has been previously characterized to inhibit complex III of the electron transport chain and uncouple the mitochondrial proton gradient. The purpose of this study was to analyze ATP-linked respiration and glycolysis in human neuroblastoma cells utilizing the Seahorse extracellular flux platform. Employing an acute, subtoxic exposure of MB, this investigation revealed a MB-mediated decrease in mitochondrial oxygen consumption at baseline and maximal respiration, with inhibition of ATP synthesis and coupling efficiency. Additionally, MB-treated cells showed an increase in nonmitochondrial respiration and proton leak. Further investigation into mitochondrial fuel flex revealed an elimination of fuel flexibility across all 3 major substrates, with a decrease in pyruvate capacity as well as glutamine dependency. Analyses of glycolytic function showed a substantial decrease in glycolytic acidification caused by lactic acid export. This inhibition of glycolytic parameters was also observed after titrating the MB dose as low as 6 μM, and appears to be dependent on the dithiocarbamate functional group, with manganese possibly potentiating the effect. Further studies into cellular ATP and NAD levels revealed a drastic decrease in cells treated with MB. In summary, MB significantly impacted both aerobic and anaerobic energy production; therefore, further characterization of MB's effect on cellular energetics may provide insight into the specificity of PD to dopaminergic neurons.
TFAP2A upregulates SKA3 to promote glycolysis and reduce the sensitivity of lung adenocarcinoma cells to cisplatin
<p>Supplementary data for the article</p>
Autophagy Maintains Vascular Function Through a Novel Glycolysis-linked Pathway Regulating eNOS
ClinicalTrials.gov study NCT04200560. IPD Sharing: YES. Countries: 1. Publications: 0.
Data from: Acute maneb exposure significantly alters both glycolysis and mitochondrial function in neuroblastoma cells
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The Long Noncoding RNA Lncenc1 Regulates Glycolysis in Naive Mouse ES Cells II
GEO Series GSE116462. Mus musculus. 4 samples. Type: Expression profiling by high throughput sequencing.
Further inhibition of Histone H2A ubiquitination protects myocardium against ischemia/reperfusion injury through enhancing glycolysis and improving mitochondrial function via promoting Hsp27 expressio
GEO Series GSE225245. Rattus norvegicus. 6 samples. Type: Expression profiling by high throughput sequencing.
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