ArticleBMB reports2019
Defect of SIRT1-FoxO3a axis is associated with the production of reactive oxygen species during protein kinase CK2 downregulation-mediated cellular senescence and nematode aging.
Article in BMB reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Pathological, diagnostic, and therapeutic implications of non-coding RNAs in deep vein thrombosis: A comprehensive review.Journal of thrombosis and thrombolysis · 2026Review
- AMPK/SIRT1/PGC-1α Signaling Pathway: Molecular Mechanisms and Targeted Strategies From Energy Homeostasis Regulation to Disease Therapy.CNS neuroscience & therapeutics · 2025Review
- Ovarian Aging: The Silent Catalyst of Age-Related Disorders in Female Body.Aging and disease · 2025Review
- Protein Kinase CK2 Is Upregulated by Calorie Restriction and Induces Autophagy.Molecules and cells · 2022Article
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- Suppression ofBiomolecules & therapeutics · 2021Article
- Oxidative Stress, Diet and Prostate Cancer.The world journal of men's health · 2021Review
- Review
- Article
- CK2 Down-Regulation Increases the Expression of Senescence-Associated Secretory Phenotype Factors through NF-κB Activation.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We investigated whether SIRT1 is associated with reactive oxygen species (ROS) accumulation during CK2 downregulationmediated senescence. SIRT1 overexpression suppressed ROS accumulation, reduced transcription of FoxO3a target genes, and nuclear export and acetylation of FoxO3a, which were induced by CK2 downregulation in HCT116 and MCF-7 cells. Conversely, overexpression of a dominant-negative mutant SIRT1 (H363Y) counteracted decreased ROS levels, increased transcriptional activity of FoxO3a, and increased nuclear import and decreased acetylation of FoxO3a, which were induced by CK2 upregulation. CK2 downregulation destabilized SIRT1 protein via an ubiquitin-proteasome pathway in human cells, whereas CK2 overexpression reduced ubiquitination of SIRT1. Finally, the SIRT1 activator resveratrol attenuated the accumulation of ROS and lipofuscin as well as lifespan shortening, and reduced expression of the DAF-16 target gene sod-3, which were induced by CK2 downregulation in nematodes. Altogether, this study demonstrates that inactivation of the SIRT1-FoxO3a axis, at least in part, is involved in ROS generation during CK2 downregulationmediated cellular senescence and nematode aging. [BMB Reports 2019; 52(4): 265-270].
Indexed as
Identifiers
30103847PMC6507845W2942739638What OpenQuestion holds
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.