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AMPK is necessary for Treg functional adaptation to microenvironmental stress during malignancy and viral pneumonia

ABSTRACT: AMPK is necessary for Treg functional adaptation to microenvironmental stress during malignancy and viral pneumonia

PROVIDER: PRJNA1047023 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27002258.fastq.gz	Fastqsanger.gz
	SRR27002259.fastq.gz	Fastqsanger.gz
	SRR27002260.fastq.gz	Fastqsanger.gz
	SRR27002261.fastq.gz	Fastqsanger.gz
	SRR27002262.fastq.gz	Fastqsanger.gz

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AMPK is necessary for Treg functional adaptation to microenvironmental stress during malignancy and viral pneumonia

Project description:AMPK is necessary for Treg functional adaptation to microenvironmental stress during malignancy and viral pneumonia

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AMPK is necessary for Treg functional adaptation to microenvironmental stress during malignancy and viral pneumonia

Project description:AMPK is necessary for Treg functional adaptation to microenvironmental stress during malignancy and viral pneumonia

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AMPK is necessary for Treg functional adaptation to microenvironmental stress during malignancy and viral pneumonia

Project description:CD4+FOXP3+ regulatory T (Treg) cells maintain self-tolerance, suppress the immune response to cancer, and protect against tissue injury in the lung and other organs. Treg cells require mitochondrial metabolism to exert their function, but how Treg cells adapt their metabolic programs to sustain and optimize their function during an immune response occurring in a metabolically stressed microenvironment remains unclear. Here, we tested whether Treg cells require the energy homeostasis-maintaining enzyme AMP-activated protein kinase (AMPK) to adapt to metabolically aberrant microenvironments caused by malignancy or lung injury, finding that AMPK is dispensable for Treg cell immune-homeostatic function but is necessary for full Treg cell function in B16 melanoma tumors and during acute lung injury caused by influenza virus pneumonia. AMPK-deficient Treg cells had lower mitochondrial mass and exhibited an impaired ability to maximize aerobic respiration. Mechanistically, we found that AMPK regulates DNA methyltransferase 1 to promote transcriptional programs associated with mitochondrial function in the tumor microenvironment. In the lung during viral pneumonia, we found that AMPK sustains metabolic homeostasis and mitochondrial activity. Induction of DNA hypomethylation was sufficient to rescue mitochondrial mass in AMPK-deficient Treg cells, linking DNA methylation with AMPK function and mitochondrial metabolism. These results define AMPK as a determinant of Treg cell adaptation to metabolic stress and offer potential therapeutic targets in cancer and tissue injury.

2025-03-19 | GSE249017 | GEO

AMPK is necessary for Treg functional adaptation to microenvironmental stress during malignancy and viral pneumonia

2025-03-19 | GSE249018 | GEO

AMPK is necessary for Treg functional adaptation to microenvironmental stress during malignancy and viral pneumonia

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

2025-03-19 | GSE249019 | GEO

Oncostatin M neutralization in E. coli pneumonia

Project description:Oncostatin M (OSM) is an IL-6 family cytokine that is necessary for neutrophil recruitment in pneumonia by inducing STAT3-dependent production of CXCL5. We used microarrays to identify additional pathways affected by OSM neutralization in the lungs during pneumonia.

2021-03-08 | GSE155283 | GEO

Mouse livers during pneumonia

Project description:This SuperSeries is composed of the following subset Series: GSE32105: Expression data from mouse livers lacking STAT3 and RelA during pneumonia GSE35513: Expression data from mouse livers lacking NF-kappaB RelA (p65) during pneumonia GSE35514: Expression data from mouse livers lacking STAT3 during pneumonia GSE35515: Expression data from mouse livers expressing or lacking Cre recombinase during pneumonia Refer to individual Series

2012-02-16 | E-GEOD-35516 | biostudies-arrayexpress

AMPK-dependent activation of the Cyclin Y/CDK16 complex controls autophagy

Project description:The AMP-activated protein kinase (AMPK) is a master sensor of the cellular energy status and is crucial for the adaptive response to limited energy availability. AMPK is implicated in the regulation of many cellular processes, including autophagy. However, the precise mechanisms by which AMPK controls these processes and the identities of relevant substrates are not fully understood. With a protein microarrays we identified Cyclin Y as novel AMPK substrate that is phosphorylated at S326 both in vitro and in cells. Phosphorylation of Cyclin Y at S326 promotes its interaction with the cyclin-dependent kinase 16 (CDK16), thereby stimulating its catalytic activity. When expressed in cells, Cyclin Y/CDK16 is sufficient to promote autophagy. Moreover, Cyclin Y/CDK16 is necessary for efficient AMPK-dependent activation of autophagy. This functional interaction is mediated by AMPK phosphorylating S326 of Cyclin Y. Collectively, we define Cyclin Y/CDK16 as downstream effector of AMPK for inducing autophagy.

2020-02-17 | PXD009968 | Pride

Expression data from AMPK deficient MLL-AF9 leukemia initiating cells and whole leukemia cells

Project description:Deletion of AMPK significantly extended the onset of leukemogenesis and depleted leukemia initiating cells (LICs). To identify how AMPK regulates LICs, we performed gene expression profiling of LICs isolated from AMPK wild type leukemic mice or AMPK-deficient leukemic mice. 4 groups were analyzed; 1) Whole leukemia (GFP+) from AMPK WT ( AMPKfl/fl) mice, 2) Whole leukemia (GFP+) from AMPK-deficient ( AMPK?/?l) mice, 3) LICs=L-GMP (GFP+,lin-,c-kit+, CD16/32+,CD34+) cells from AMPK WT ( AMPKfl/fl) mice, 4) LICs=L-GMP (GFP+,lin-,c-kit+, CD16/32+,CD34+) cells from AMPK-deficient ( AMPK?/?l) mice.

2015-01-01 | E-GEOD-64602 | biostudies-arrayexpress

AMPK-dependent gene expression profiles in response to small molecule AMPK activators

Project description:AMP-activated protein kinase (AMPK) is a major regulator of cellular energy homeostasis that coordinates metabolic pathways in order to balance nutrient supply with energy demand. AMPK elicits acute and diverse metabolic effects by directly phosphorylating various targets. AMPK activation also promotes metabolic reprogramming in longer term via effects on gene expression. The aim of this study is to elucidate molecular mechanism(s) by which AMPK activation modulates metabolic adaptation through its impact on gene regulation.

2019-03-04 | GSE104170 | GEO

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