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443 results for “Metabolic Reprogramming”
Single cell transcriptomics unveiled that early life BDE-99 exposure reprogrammed the gut-liver axis to promote a pro-inflammatory metabolic signature in male mice at late adulthood (Part 1/2)
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Single cell transcriptomics unveiled that early life BDE-99 exposure reprogrammed the gut-liver axis to promote a pro-inflammatory metabolic signature in male mice at late adulthood (Part 2/2)
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Metabolic data: Inhibition of mitochondrial complex I reverses NOTCH1-driven metabolic reprogramming in T-cell acute lymphoblastic leukemia
<p>T-cell acute lymphoblastic leukemia (T-ALL) is commonly driven by activating mutations in <em>NOTCH1 </em>that facilitate glutamine oxidation. Here we identify oxidative phosphorylation (OxPhos) as a critical pathway for leukemia cell survival and demonstrate a direct relationship between <em>NOTCH1</em>, elevated OxPhos gene expression, and acquired chemoresistance in pre-leukemic and leukemic models. Disrupting OxPhos with IACS-010759, an inhibitor of mitochondrial complex I, causes potent growth inhibition through induction of metabolic shut-down and redox imbalance in <em>NOTCH1</em>-mutated and less so in <em>NOTCH1</em>-wt T-ALL cells. Mechanistically, inhibition of OxPhos induces metabolic reprogramming into glutaminolysis. We show that pharmacological blockade of OxPhos combined with inducible knock-down of glutaminase, the key glutamine enzyme, confers synthetic lethality in mice harboring <em>NOTCH1</em>-mutated T-ALL<em>. </em>We leverage this synthetic lethal interaction to demonstrate that IACS-010759 in combination with chemotherapy containing L-asparaginase, an enzyme that uncovers the glutamine dependency of leukemic cells, causes reduced glutaminolysis and profound tumor reduction in pre-clinical models of human T-ALL. In summary, this metabolic dependency of T-ALL on OxPhos provides a rational therapeutic target.</p>
Intergrated Multi-omics Sequencing Reveals Metabolic Reprograms in the Progression of ccRCC
<p>ccRCC is a complex disease with remarkable immune and metabolic heterogeneity. Here, we present a TJ-RCC cohort, performing genomic, transcriptomic, proteomic, metabonomic and spatial multi-omic profiling on 100 ccRCC cases. Using the scRNA-seq-derived signature, we identify 4 subtypes. Multilevel profiling distinguishes a unique ccRCC subtype, De-clear cell differentiated (DCCD) -ccRCC, with distinctive metabolic features. DCCD cancer cells are characterized by fewer lipid droplets, extremely inhibited metabolic activity, enhanced nutrients uptake capability and a high proliferation rate, leading to poor prognosis. Using single-cell and spatial trajectory analysis, we demonstrate that DCCD is a common mode of ccRCC progression. Even among stage I patients, DCCD indicates worse outcomes and higher recurrence rate, indicating it cannot be cured by nephrectomy alone. This study provides a treatment strategy based on immune subtypes, which could enable precise clinical management of ccRCC.</p>
High Fat Diet for Cardiac Metabolic Reprogramming
ClinicalTrials.gov study NCT06747429. IPD Sharing: NO. Countries: 0. Publications: 13.
Data from: Enhanced resistance to <em>Listeria</em> infection in mice surviving sepsis: The role of lipid metabolism and myeloid cell reprogramming
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Patient-derived organotypic tissue cultures as a platform to evaluate metabolic reprogramming in breast cancer patients
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TGFβRI modulates metabolic reprogramming via the aPKC-PEPCK axis during pupal diapause in the cotton Bollworm, <em>Helicoverpa armigera</em>
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Human airway macrophages are metabolically reprogrammed by IFN-γ resulting in glycolysis-dependent functional plasticity
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Intracellular sodium elevation reprograms cardiac metabolism: Metabolomics data
<p><span><span><span><span><span><span><span><span><span><span><span>Intracellular Na elevation in the heart is a hallmark of pathologies where both acute and chronic metabolic remodeling occurs. We assessed whether acute (75μM ouabain 100nM blebbistatin) and chronic myocardial Na<sub>i</sub>load (PLM<sup>3SA </sup>mouse) are causally linked to metabolic remodeling and whether the hypertrophied failing heart shares a common Na-mediated metabolic 'fingerprint'. Control (PLM<sup>WT</sup>), transgenic (PLM<sup>3SA</sup>), ouabain treated and hypertrophied Langendorff-perfused mouse hearts were studied by <sup>23</sup>Na, <sup>31</sup>P, <sup>13</sup>C NMR followed by <sup>1</sup>H NMR metabolomic profiling. Elevated Na<sub>i</sub> leads to <i><u>common </u></i>adaptive metabolic alterations preceding energetic impairment: a switch from fatty acid to carbohydrate metabolism and changes in steady-state metabolite concentrations (glycolytic, anaplerotic, Krebs cycle intermediates). Inhibition of mitochondrial Na/Ca exchanger by CGP37157 ameliorated the metabolic changes. <i>In silico</i> modelling indicated altered metabolic fluxes (Krebs cycle, fatty acid, carbohydrate, amino acid metabolism). Prevention of Na<sub>i</sub> overload or inhibition of Na/Ca<sub>mito</sub>may be a new approach to ameliorate metabolic dysregulation in heart failure.</span></span></span></span></span></span></span></span></span></span></span></p>
Intestinal Metabolic Reprogramming as a Key Mechanism of Gastric Bypass in Humans
ClinicalTrials.gov study NCT02710370. IPD Sharing: UNDECIDED. Countries: 1. Publications: 9.
Intracellular sodium elevation reprograms cardiac metabolism: Metabolomics data
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Deep learning reveals the metabolic dependency of hypoxic tumor cells and the critical function of FLAD1 mediated mitochondrial metabolic reprogramming
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Paternally-induced transgenerational environmental reprogramming of metabolic gene expression in mammals (small RNA)
GEO Series GSE25897. Mus musculus. 8 samples. Type: Non-coding RNA profiling by high throughput sequencing.
Disruption of Cytochrome c Oxidase Function Induces Warburg Effect and Metabolic Reprogramming
GEO Series GSE68525. Mus musculus. 6 samples. Type: Expression profiling by array.
Immunoediting instructs tumor metabolic reprogramming to support immune evasion [smartseq]
GEO Series GSE217862. Mus musculus. 6 samples. Type: Expression profiling by high throughput sequencing.
Metabolic reprogramming of macrophage polarization by creatine [RNA-seq]
GEO Series GSE110395. Mus musculus. 8 samples. Type: Expression profiling by high throughput sequencing.
Disrupted Macrophage Metabolic Reprogramming in Aged Soleus Muscle During Early Recovery following Disuse Atrophy
GEO Series GSE158987. Mus musculus. 6 samples. Type: Expression profiling by high throughput sequencing.
Spatial Multiomics Reveals Metabolic Reprogramming and Calcification Characteristics of Diabetic Macroangiopathy [scRNA-Seq]
GEO Series GSE248609. Homo sapiens. 6 samples. Type: Expression profiling by high throughput sequencing.
Immunoediting instructs tumor metabolic reprogramming to support immune evasion [Bisulfite-seq]
GEO Series GSE217481. Mus musculus. 6 samples. Type: Methylation profiling by high throughput sequencing.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.