ATM is a key driver of NF-κB-dependent DNA-damage-induced senescence, stem cell dysfunction and aging
Open accessAbstract
mice with the ATM inhibitor KU-55933 suppressed markers of senescence and SASP. Taken together, these results demonstrate that the ATM kinase is a major mediator of DNA damage-induced, NF-κB-mediated cellular senescence, stem cell dysfunction and aging and thus represents a therapeutic target to slow the progression of aging.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
ATM is known to be the key driver of DNA-damage induced senescence.
“ZFP36L2, ZFP36L1 are associated with SASP and ATM is known to be the key driver of DNA-damage induced senescence [82].”
From Characterisation of premature cell senescence in Alzheimer's disease using single nuclear transcriptomics (2024) · cites this paper as [82]
ZFP36L2 and ZFP36L1 are associated with SASP.
“ZFP36L2, ZFP36L1 are associated with SASP and ATM is known to be the key driver of DNA-damage induced senescence [82].”
From Characterisation of premature cell senescence in Alzheimer's disease using single nuclear transcriptomics (2024) · cites this paper as [82]
The Discussion supports an ATM–NF-κB–SASP connection, but it does not link ZFP36L2 or ZFP36L1 to SASP. Searches for both gene names in our copy returned no matching passage, so the specific claim about those genes cannot be verified from this source. (LLM, conf=0.76)
Experimental — accuracy not yet measuredIκB degradation allows NF-κB translocation into the nucleus where it transactivates several SASP genes.
“IκB degradation allows NF-κB translocation into the nucleus where it transactivates several SASP genes [156,157].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [157]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 80 · Cited by 122
Research works printed but not linked: 2
- [60]Hertlein E, Wang J, Ladner KJ, Bakkar N, Guttridge DC. RelA/p65 regulation of IkappaBbeta. Mol Cell Biol. 2005; 25: 4956– 68. 10.1128/MCB.25.12.4956-4968.2005 15923614 PMC1140602 · DOI
- [80]Qu-Petersen Z, Deasy B, Jankowski R, Ikezawa M, Cummins J, Pruchnic R, Mytinger J, Cao B, Gates C, Wernig A, Huard J. Identification of a novel population of muscle stem cells in mice: potential for muscle regeneration. J Cell Biol. 2002; 157: 851– 64. 10.1083/jcb.200108150 12021255 PMC2173424 · DOI
- Authors
- Zhao, J., Zhang, L., Lu, A., Han, Y., Colangelo, D., Bukata, C., Scibetta, A., Yousefzadeh, M. J., Li, X., Gurkar, A. U., McGowan, S. J., Angelini, L., O’Kelly, R., Li, H., Corbo, L., Sano, T., Nick, H., Pola, E., Pilla, S. P. S., Ladiges, W. C., Vo, N., Huard, J., Niedernhofer, L. J., & Robbins, P. D.
- Affiliations
- University of Minnesota (US)
- Steadman Philippon Research Institute (US)
- University of Pittsburgh (US)
- Agostino Gemelli University Polyclinic (IT)
- Department of Molecular Medicine and the Center on Aging, Scripps Research, Jupiter, FL 33458, USA
- University of Washington (US)
- Corresponding author
- Robbins, Paul D.
- ORCID
- Venue
- Aging
- Publisher
- Impact Journals, LLC
- Published
- 2020-03-22
- Volume
- 12
- Issue
- 6
- Pages
- 4688-4710
- ISSN
- 1945-4589 (ISSN-L)
- PMC
- PMC7138542
- OpenAlex
- W3012572174
- Cited by
- 122
- References
- 80
- Citations by year
- 2026: 18 · 2025: 26 · 2024: 26 · 2023: 14 · 2022: 16 · 2021: 18 · 2020: 4
- FWCI
- 7.82
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- cc-by
- Locations
- Aging (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- PubliCatt (Università Cattolica del Sacro Cuore) (submittedVersion, cc-by)
- Funders
- National Institute on Aging (R00AG049126, P01AG043376, R01AG044376, R56AG059676, P30AG024827, U19AG056278, P01AG062413, R01AG063543)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Keywords
- ATM kinase, NF-κB, DNA damage-induced senescence, cellular senescence, stem cell dysfunction, senescence-associated secretory phenotype, KU55933, senolytic therapy
- MeSH terms
- Aging, Animals, Cells, Cultured, DNA Damage, DNA-Binding Proteins, Endonucleases, Mice, Inbred C57BL, Stem Cells, NF-kappa B, Cellular Senescence, Mice, Knockout, Ataxia Telangiectasia Mutated Proteins
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
