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Ablation of DNA-methyltransferase 3A in skeletal muscle does not affect energy metabolism or exercise capacity [RRBS]

ABSTRACT: Ablation of DNA-methyltransferase 3A in skeletal muscle does not affect energy metabolism or exercise capacity [RRBS]

PROVIDER: PRJNA639068 | ENA |

REPOSITORIES: ENA

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Ablation of DNA-methyltransferase 3A in skeletal muscle does not affect energy metabolism or exercise capacity [RRBS]

Project description:Skeletal muscle can undergo large transcriptional changes in response to environmental stimuli such as diet or exercise in order to adapt to energetic demands. This remodelling has been associated with changes in muscle DNA methylation potentially regulating gene transcription. Despite abundant evidence that environmental stimuli can alter muscle DNA methylation, the mechanisms by which DNA methylation machinery respond to these stimuli and whether these have a physiological impact is still unclear. Therefore, we decided to investigate the importance of de novo DNA methylation on muscle methylation and function. We generated muscle specific DNMT3a knockout mice (mDKO) and investigated the impact of ablating DNMT3a in muscle on muscle DNA methylation, exercise capacity and energy metabolism. Loss of DNMT3a reduced DNA methylation in muscle over multiple genomic contexts and altered the transcription of genes known to be influenced by DNA methylation. However, mDKO mice had a similar exercise capacity and whole-body energy metabolism as WT mice. Similarly, loss of DNMT3a did not alter muscle mitochondrial function or the transcriptional response to exercise however did increase the expression of genes involved in muscle development. These data suggest that DNMT3a does not have a large role in the function of mature muscle although a role in muscle development and differentiation is still likely.

2021-01-25 | GSE152348 | GEO

Ablation of DNA-methyltransferase 3A in skeletal muscle does not affect energy metabolism or exercise capacity

Project description:Ablation of DNA-methyltransferase 3A in skeletal muscle does not affect energy metabolism or exercise capacity

| PRJNA639065 | ENA

Ablation of DNA-methyltransferase 3A in skeletal muscle does not affect energy metabolism or exercise capacity

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

2021-01-25 | GSE152349 | GEO

Ablation of DNA-methyltransferase 3A in skeletal muscle does not affect energy metabolism or exercise capacity [RNA-seq]

Project description:Ablation of DNA-methyltransferase 3A in skeletal muscle does not affect energy metabolism or exercise capacity [RNA-seq]

| PRJNA639067 | ENA

Ablation of DNA-methyltransferase 3A in skeletal muscle does not affect energy metabolism or exercise capacity.

Project description: Not available

| S-EPMC7875352 | biostudies-literature

Ablation of DNA-methyltransferase 3A in skeletal muscle does not affect energy metabolism or exercise capacity [RNA-seq]

2021-01-25 | GSE152347 | GEO

DNA Methyltransferase 3A Mediates the Sustained Effects of Stress on Synaptic Functions and Behaviors [RRBS]

Project description:DNA Methyltransferase 3A Mediates the Sustained Effects of Stress on Synaptic Functions and Behaviors [RRBS]

| PRJNA622272 | ENA

Transcriptionally regulated energy metabolism drives early erythropoiesis (RRBS)

Project description:Transcriptionally regulated energy metabolism drives early erythropoiesis (RRBS)

| PRJNA686370 | ENA

GSK-3A and GSK-3B knockdown in AML cell lines

Project description:Gene expression data from AML cell lines, MOLM-14, U937, THP-1 and HL-60, that were infected with a scrambled control hairpin (shControl), two shRNAs directed against GSK-3B (shGSK3B_1 and shGSK3B_2), or two shRNAs directed against GSK-3A (shGSK3A_5 and shGSK3A_6). Acute myeloid leukemia (AML) is the most common form of acute leukemia in adults. Long-term survival of patients with AML has changed little over the past decade, necessitating the identification and validation of new AML targets. Integration of genomic approaches with small-molecule and genetic-based high-throughput screening holds the promise of improved discovery of candidate targets for cancer therapy. Here, we identified a role for glycogen synthase kinase 3A (GSK-3A) in AML by performing two independent small-molecule library screens and an shRNA screen for perturbations that induced a differentiation expression signature in AML cells. GSK-3 is a serine-threonine kinase involved in diverse cellular processes including differentiation, signal transduction, cell cycle regulation, and proliferation. We demonstrated that specific loss of GSK-3A induced differentiation in AML by multiple measurements, including induction of gene expression signatures, morphological changes, and cell surface markers consistent with myeloid maturation. GSK-3AM-bM-^@M-^Sspecific suppression also led to impaired growth and proliferation in vitro, induction of apoptosis, loss of colony formation in methylcellulose, and anti-AML activity in vivo. Although the role of GSK-3B has been well studied in cancer development, these studies support a role for GSK-3A in AML. The AML cell lines, MOLM-14, U937, THP-1 and HL-60, were infected with a scrambled control hairpin (shControl), two shRNAs directed against GSK-3B (shGSK3B_1 and shGSK3B_2), and two shRNAs directed against GSK-3A (shGSK3A_5 and shGSK3A_6).

2012-02-27 | E-GEOD-35200 | biostudies-arrayexpress

Expression data from human sarcoma patient samples treated with either vehicle control or Nutlin-3a

Project description:This study has examined the molecular mechanisms underlying sensitivity of sarcomas to Nutlin-3a, a non-genotoxic activator of the p53 pathway. Human patient material was collected immediately following surgical resection, dissected into small pieces and ex planted onto gelatin sponges immersed in media containing either vehicle control or Nutlin-3a (10uM and/or 50uM) for 48 hours. Nutlin-3a represents a novel targeted therapy for the treatment of sarcomas. We have examined expression profiles of genes upregulated in sarcoma patient derived tissues following nutlin-3a treatment ex vivo 16 samples ((Vehicle control and Nutlin-3a (10uM and 50uM) treated samples)) from 6 sarcoma patients

2014-03-10 | E-GEOD-48296 | biostudies-arrayexpress

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