ArticleBMC biochemistry2016
Sustained activation of mTORC1 in macrophages increases AMPKα-dependent autophagy to maintain cellular homeostasis.
Article in BMC biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 26 citations in OpenAlex.
- mTOR Signaling in Macrophages: All Depends on the Context.International journal of molecular sciences · 2025Review
- The Role of mTOR inBiomedicines · 2024Review
- Reprogramming tumor-associated macrophages to outcompete endovascular endothelial progenitor cells and suppress tumor neoangiogenesis.Immunity · 2023Article
- Chronic exposure to carbon black ultrafine particles reprograms macrophage metabolism and accelerates lung cancer.Science advances · 2022Article
- Article
- Genetic context of oncogenic drivers dictates vascular sarcoma development in aP2-Cre mice.The Journal of pathology · 2022Article
- The Amino Acid-mTORC1 Pathway Mediates APEC TW-XM-Induced Inflammation in bEnd.3 Cells.International journal of molecular sciences · 2021Article
- Regulation of Intrinsic and Bystander T Follicular Helper Cell Differentiation and Autoimmunity by Tsc1.Frontiers in immunology · 2021Article
- Article
- Enhanced translation expands the endo-lysosome size and promotes antigen presentation during phagocyte activation.PLoS biology · 2019Article
- TSC1 and TSC2 regulate cilia length and canonical Hedgehog signaling via different mechanisms.Cellular and molecular life sciences : CMLS · 2018Article
- mTOR independent alteration in ULK1 Ser758 phosphorylation following chronic LRRK2 kinase inhibition.Bioscience reports · 2018Article
- Regulation of Metabolic Disease-Associated Inflammation by Nutrient Sensors.Mediators of inflammation · 2018Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe mechanistic target of rapamycin complex 1 (mTORC1) is a well-conserved serine/threonine protein kinase that controls autophagy as well as many other processes such as protein synthesis, cell growth, and metabolism. The activity of mTORC1 is stringently and negatively controlled by the tuberous sclerosis proteins 1 and 2 complex (TSC1/2).
resultsIn contrast to the previous studies using Tsc1 knockout mouse embryonic fibroblasts (MEF) cells, we demonstrated evidence that TSC1 deficient macrophages exhibited enhanced basal and mycobacterial infection-induced autophagy via AMPKα-dependent phosphorylation of ULK1 (Ser555). These effects were concomitant with constitutive activation of mTORC1 and can be reversed by addition of amino acids or rapamycin, and by the knockdown of the regulatory-associated protein of mTOR, Raptor. In addition, increased autophagy in TSC1 deficient macrophages resulted in suppression of inflammation during mycobacterial infection, which was reversed upon amino acid treatment of the TSC1 deficient macrophages. We further demonstrated that TSC1 conditional knockout mice infected with Mycobacterium tuberculosis, the causative agent of tuberculosis, resulted in less bacterial burden and a comparable level of inflammation when compared to wild type mice.
conclusionsOur data revealed that sustained activation of mTORC1 due to defects in TSC1 promotes AMPKα-dependent autophagic flux to maintain cellular homeostasis.
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