ArticleThe Journal of biological chemistry2009
Oxidative stress is linked to ERK1/2-p16 signaling-mediated growth defect in ATM-deficient astrocytes.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 74 citations in OpenAlex.
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- Nacre Extract from Pearl Oyster Shell Prevents D-Galactose-Induced Brain and Skin Aging.Marine biotechnology (New York, N.Y.) · 2023Article
- P16INK4A-More Than a Senescence Marker.Life (Basel, Switzerland) · 2022Review
- ATM: Functions of ATM Kinase and Its Relevance to Hereditary Tumors.International journal of molecular sciences · 2022Review
- An anaplerotic approach to correct the mitochondrial dysfunction in ataxia-telangiectasia (A-T).Molecular metabolism · 2021Article
- Cellular functions of the protein kinase ATM and their relevance to human disease.Nature reviews. Molecular cell biology · 2021Review
- ATM at the crossroads of reactive oxygen species and autophagy.International journal of biological sciences · 2021Review
- Mitochondria at the crossroads of ATM-mediated stress signaling and regulation of reactive oxygen species.Redox biology · 2020Review
- Cerebellar Astrocytes: Much More Than Passive Bystanders In Ataxia Pathophysiology.Journal of clinical medicine · 2020Review
- TGF-β1/IL-11/MEK/ERK signaling mediates senescence-associated pulmonary fibrosis in a stress-induced premature senescence model of Bmi-1 deficiency.Experimental & molecular medicine · 2020Article
- JNK inhibition blocks piperlongumine-induced cell death and transcriptional activation of heme oxygenase-1 in pancreatic cancer cells.Apoptosis : an international journal on programmed cell death · 2019Article
- Oxidized ATM-mediated glycolysis enhancement in breast cancer-associated fibroblasts contributes to tumor invasion through lactate as metabolic coupling.EBioMedicine · 2019Article
- PQM130, a Novel Feruloyl-Donepezil Hybrid Compound, Effectively Ameliorates the Cognitive Impairments and Pathology in a Mouse Model of Alzheimer's Disease.Frontiers in pharmacology · 2019Article
- Mitochondrial redox sensing by the kinase ATM maintains cellular antioxidant capacity.Science signaling · 2018Article
- Inflammation, a significant player of Ataxia-Telangiectasia pathogenesis?Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018Review
- An Effective Epigenetic-PARP Inhibitor Combination Therapy for Breast and Ovarian Cancers Independent of BRCA Mutations.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
- ATM is required for SOD2 expression and homeostasis within the mammary gland.Breast cancer research and treatment · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The gene that encodes the ATM protein kinase is mutated in ataxia-telangiectasia (A-T). One of the prominent features of A-T is progressive neurodegeneration. We have previously reported that primary astrocytes isolated from Atm(-/-) mice grow slowly and die earlier than control cells in culture. However, the mechanisms for this remain unclear. We show here that intrinsic elevated intracellular levels of reactive oxygen species (ROS) are associated with the senescence-like growth defect of Atm(-/-) astrocytes. This condition is accompanied by constitutively higher levels of ERK1/2 phosphorylation and p16(Ink4a) in Atm(-/-) astrocytes. We also observe that ROS-induced up-regulation of p16(Ink4a) occurs correlatively with ERK1/2-dependent down-regulation and subsequent dissociation from chromatin of Bmi-1. Furthermore, both mitogen-activated protein kinase (MAPK)/ERK inhibitor PD98059 and antioxidant N-acetyl-l-cysteine restored normal proliferation of Atm(-/-) astrocytes. These results suggest that ATM is required for normal astrocyte growth through its ability to stabilize intracellular redox status and that the inability to control ROS is the molecular basis of limited cell growth of Atm(-/-) astrocytes. This defect may be mediated by a mechanism involving ERK1/2 activation and Bmi-1 derepression of p16(Ink4a). These data identify new potential targets for therapeutic intervention in A-T neurodegeneration.
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