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Licochalcone A activate glycolysis by via PI3K / AKT pathway to play an anti-aging effect on adipose stem cells and aging mice [hADSCs]

ABSTRACT: Licochalcone A activate glycolysis by via PI3K / AKT pathway to play an anti-aging effect on adipose stem cells and aging mice [hADSCs]

PROVIDER: PRJNA602840 | ENA |

REPOSITORIES: ENA

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Licochalcone A activate glycolysis by via PI3K / AKT pathway to play an anti-aging effect on adipose stem cells and aging mice

Project description:Licochalcone A activate glycolysis by via PI3K / AKT pathway to play an anti-aging effect on adipose stem cells and aging mice

| PRJNA602830 | ENA

Licochalcone A activate glycolysis by via PI3K / AKT pathway to play an anti-aging effect on adipose stem cells and aging mice [hippocampus]

Project description:Licochalcone A activate glycolysis by via PI3K / AKT pathway to play an anti-aging effect on adipose stem cells and aging mice [hippocampus]

| PRJNA602809 | ENA

Licochalcone A activate glycolysis by via PI3K / AKT pathway to play an anti-aging effect on adipose stem cells and aging mice [hADSCs]

Project description:We implemented transcriptomic analyses of hADSCs treated with Licochalcone A 6 days

2022-01-21 | GSE144122 | GEO

Licochalcone A activate glycolysis by via PI3K / AKT pathway to play an anti-aging effect on adipose stem cells and aging mice [hippocampus]

Project description:We implemented transcriptomic analyses of hippocampus of 12M mice; These mice with the treatment of Licochalcone A for 30 days.

2022-01-10 | GSE144105 | GEO

Licochalcone A activate glycolysis by via PI3K / AKT pathway to play an anti-aging effect on adipose stem cells and aging mice

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-01-10 | GSE144123 | GEO

Epigenetic Drift of H3K27me3 in Aging Links Glycolysis to Healthy Longevity

Project description:We adapted ChIP-Rx method established in cells to fly tissues for quantitative ChIP-seq. We found the deposition of H3K27me3 during aging loses fidelity, resulting its propagation across the epigenome; lowering H3K27me3 by PRCs-deficiency promotes healthy lifespan by mitigating this trend. Quantitative multi-omic analysis converges on a central role of glycolysis, linking H3K27me3 dynamics to the regulation of glycolytic genes, which correspondingly rewire cellular metabolic homeostasis including energy and redox potential that impact lifespan and adult fitness.

2018-06-04 | GSE96654 | GEO

Aging of mouse spermatogonial stem cells by Wnt7b-Jnk pathway activation [ChIP-seq]

Project description:Because spermatogonial stem cells (SSCs) are virtually immortal by serial transplantation, SSC decrease in aged testes is considered to be caused by deteriorated microenvironment. Here we report cell-intrinsic mode of SSC aging. SSCs cultured for 5 years proliferate more actively than young SSCs and showed enhanced glycolytic activity but remain euploid and exhibited stable androgenetic imprinting patterns. Moreover, the aged SSCs kept constant SSC activity despite shortened telomeres. The increased proliferative activity of aged SSCs was caused by Wnt7b expression, which likely occurred due to decreased polycomb complex2 activity. Aberrant Wnt7b expression not only decreased reactive oxygen species levels and mitochondria activity but also stimulated glycolysis via c-jun N-terminal kinase (JNK) activation. Analysis of SSCs in Klotho aging mouse model also confirmed hyperactivation of JNK pathway and increased glycolysis. Therefore, not only SSC microenvironment but also intrinsic activation of Wnt7b-mediated glycolysis plays important roles in SSC aging.

2019-07-30 | GSE120777 | GEO

Aging of mouse spermatogonial stem cells by Wnt7b-Jnk pathway activation [Bisulfite-seq]

2019-07-30 | GSE120775 | GEO

Methan producing activate sludge

Project description:Methan producing activate sludge Metagenome

| PRJNA812233 | ENA

Combinatorial targeting of glycolysis and oxidative phosphorylation suppresses tumor growth and metastases.

Project description:The Warburg effect, consisting of increased glucose uptake and glycolysis, provides metabolic energy as well as cellular building blocks for tumor growth. Inhibition of the Warburg effect with 2-deoxyglucose (2DG) has been explored in clinical trials with limited efficacy. Blockage of glycolysis can induce autopahgy resulting in alternative energy generation through oxidative phosphorylation providing a potential bypass of the effects of inhibition of glycolysis. Here in we demonstrate that activation of AMPK, as a consequence of energetic stress, induces mitochondrial energy production potentially bypassing the effects of glycolysis inhibition. We thus combined blockage of glycolysis by 2DG with inhibition of the electron transfer complex I (ETC1) in the mitochondria with the clinically applicable antidiabetic drug metformin. The combination resulted in activation of AMPK and autopahgy that however rendered eventual depletion of ATP and cell death. Furthermore, combined inhibition of glycolysis and mitochondrial respiration inhibited tumor growth and markedly decreased metastatic capacity in vivo. In order to understand the mechanism of these metabolic inhibitors, we performed whole genome transcriptional analysis. Human SK-4 esophageal cancer cell lines were treated with 5 different treatment groups [2 deoxy glucose (4mM), Metformin (5mM), AICAR (2mM), 2 deoxy glucose (4mM) plus Metformin (5mM) and 2 deoxy glucose (4mM) plus AICAR (2mM)] with non treated control groups for 12 hrs. Each groups was quadruplicated. Microarray experiments and data analysis were done at Dept. of Systems Biology, MDACC (Houston, USA)

2012-12-31 | E-GEOD-16816 | biostudies-arrayexpress

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