ArticleBiochemical and biophysical research communications2012
Activation of AMP-activated protein kinase in cerebella of Atm-/- mice is attributable to accumulation of reactive oxygen species.
Article in Biochemical and biophysical research communications, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- Formaldehyde initiates memory and motor impairments under weightlessness condition.NPJ microgravity · 2024Review
- Pioglitazone as a Possible Treatment forBiomolecules · 2024Review
- Pathophysiological basis and promise of experimental therapies for Gulf War Illness, a chronic neuropsychiatric syndrome in veterans.Psychopharmacology · 2023Review
- JAK Inhibition Prevents DNA Damage and Apoptosis in Testicular Ischemia-Reperfusion Injury via Modulation of the ATM/ATR/Chk Pathway.International journal of molecular sciences · 2021Article
- Gulf War Illness: Mechanisms Underlying Brain Dysfunction and Promising Therapeutic Strategies.Pharmacology & therapeutics · 2021Review
- A Dual Role of ATM in Ischemic Preconditioning and Ischemic Injury.Cellular and molecular neurobiology · 2020Article
- Monosodium luminol reinstates redox homeostasis, improves cognition, mood and neurogenesis, and alleviates neuro- and systemic inflammation in a model of Gulf War Illness.Redox biology · 2020Article
- Spontaneous DNA damage to the nuclear genome promotes senescence, redox imbalance and aging.Redox biology · 2018Article
- DNA damage response in nephrotoxic and ischemic kidney injury.Toxicology and applied pharmacology · 2016Review
- Article
- ATM-Dependent Phosphorylation of All Three Members of the MRN Complex: From Sensor to Adaptor.Biomolecules · 2015Review
- The Protective Effects of Areca catechu Extract on Cognition and Social Interaction Deficits in a Cuprizone-Induced Demyelination Model.Evidence-based complementary and alternative medicine : eCAM · 2015Article
- DNA damage response in renal ischemia-reperfusion and ATP-depletion injury of renal tubular cells.Biochimica et biophysica acta · 2014Article
- Reducing mitochondrial ROS improves disease-related pathology in a mouse model of ataxia-telangiectasia.Molecular therapy : the journal of the American Society of Gene Therapy · 2013Article
- The role of the DNA damage response kinase ataxia telangiectasia mutated in neuroprotection.The Yale journal of biology and medicine · 2012Review
- Proteomic profiling of ATM kinase proficient and deficient cell lines upon blockage of proteasome activity.Journal of proteomics · 2012Article
- Targeting p38 mitogen-activated protein kinase signaling restores subventricular zone neural stem cells and corrects neuromotor deficits in Atm knockout mouse.Stem cells translational medicine · 2012Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Ataxia telangiectasia (A-T) is an inherited disease, the most prominent feature of which is ataxia caused by degeneration of cerebellar neurons and synapses. The mechanisms underlying A-T neurodegeneration are still unclear, and many factors are likely to be involved. AMP-activated protein kinase (AMPK) is a sensor of energy balance, and research on its function in neural cells has gained momentum in the last decade. The dual roles of AMPK in neuroprotection and neurodegeneration are complex, and they need to be identified and characterized. Using an Atm (ataxia telangiectasia mutated) gene deficient mouse model, we showed here that: (a) upregulation of AMPK phosphorylation and elevation of reactive oxygen species (ROS) coordinately occur in the cerebella of Atm-/- mice; (b) hydrogen peroxide induces AMPK phosphorylation in primary mouse cerebellar astrocytes in an Atm-independent manner; (c) administration of the novel antioxidant monosodium luminol (MSL) to Atm-/- mice attenuates the upregulation of both phosphorylated-AMPK (p-AMPK) and ROS, and corrects the neuromotor deficits in these animals. Together, our results suggest that oxidative activation of AMPK in the cerebellum may contribute to the neurodegeneration in Atm-/- mice, and that ROS and AMPK signaling pathways are promising therapeutic targets for treatment of A-T and other neurodegenerative diseases.
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Registered trials
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.