ArticleMolecular and cellular biochemistry2007
AICAR induces phosphorylation of AMPK in an ATM-dependent, LKB1-independent manner.
Article in Molecular and cellular biochemistry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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Who cites it
69 citing papers in PubMed, 124 citations in OpenAlex.
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- Isothiocyanates induce autophagy and inhibit protein synthesis in primary cells via modulation of AMPK-mTORC1-S6K1 signaling pathway, and protect against mutant huntingtin aggregation.European journal of nutrition · 2024Article
- Pioglitazone as a Possible Treatment forBiomolecules · 2024Review
- Mitochondrial ATP synthase as a direct molecular target of chromium(III) to ameliorate hyperglycaemia stress.Nature communications · 2023Article
- AMPK promotes Arf6 activation in a kinase-independent manner upon glucose starvation.Journal of cell science · 2022Article
- Ginsenoside compound K reduces the progression of Huntington's disease via the inhibition of oxidative stress and overactivation of the ATM/AMPK pathway.Journal of ginseng research · 2022Article
- Metformin and Cancer, an Ambiguanidous Relationship.Pharmaceuticals (Basel, Switzerland) · 2022Review
- The Tumor Suppressor Kinase LKB1: Metabolic Nexus.Frontiers in cell and developmental biology · 2022Review
- ATM Modulates Nuclear Mechanics by Regulating Lamin A Levels.Frontiers in cell and developmental biology · 2022Article
- Inducing Energetic Switching Using Klotho Improves Vascular Smooth Muscle Cell Phenotype.International journal of molecular sciences · 2021Article
- Knockdown ofBiomolecules & therapeutics · 2021Article
- Lesch-Nyhan disease causes impaired energy metabolism and reduced developmental potential in midbrain dopaminergic cells.Stem cell reports · 2021Article
- AICAR, an AMP-Activated Protein Kinase Activator, Ameliorates Acute Pancreatitis-Associated Liver Injury Partially Through Nrf2-Mediated Antioxidant Effects and Inhibition of NLRP3 Inflammasome Activation.Frontiers in pharmacology · 2021Article
- Integrin αvβ3 in the Mediating Effects of Dihydrotestosterone and Resveratrol on Breast Cancer Cell Proliferation.International journal of molecular sciences · 2020Review
- PARP1 Inhibition Augments UVB-Mediated Mitochondrial Changes-Implications for UV-Induced DNA Repair and Photocarcinogenesis.Cancers · 2019Article
- STK11 is required for the normal program of ciliated cell differentiation in airways.Cell discovery · 2019Article
- Allosteric modulation of the farnesoid X receptor by a small molecule.Scientific reports · 2018Article
9 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
AMPK is an AMP-activated protein kinase that plays an important role in regulating cellular energy homeostasis. Metabolic stress, such as heat shock and glucose starvation, causes an energy deficiency in the cell and leads to elevated levels of intracellular AMP. This results in the phosphorylation and activation of AMPK. LKB1, a tumor suppressor, has been identified as an upstream kinase of AMPK. We found that in response to treatment with 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside (AICAR), the LKB1 deficient cancer cell line, HeLa, exhibited AMPK-alpha phosphorylation. This indicates the existence of an LKB1-independent AMPK-alpha phosphorylation pathway. ATM is a protein that is deficient in the disease ataxia telangiectasia (A-T). We measured the activation of AMPK by AICAR in the normal mouse embryo fibroblast cell line, A29, and the mouse cell line lacking the ATM protein, A38. In A38 cells, the level of AICAR-induced AMPK-alpha phosphorylation was significantly lower than that found in A29 cells. Furthermore, phosphorylation of AMPK in HeLa and A29 cells was inhibited by an ATM specific inhibitor, KU-55933. Our results demonstrate that AICAR treatment could lead to phosphorylation of AMPK in an ATM-dependent and LKB1-independent manner. Thus, ATM may function as a potential AMPK kinase in response to AICAR treatment.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.