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Oxidative stress induces an ATM‐independent senescence pathway through p38 MAPK‐mediated lamin B1 accumulation
Open accessAbstract
We report crosstalk between three senescence-inducing conditions, DNA damage response (DDR) defects, oxidative stress (OS) and nuclear shape alterations. The recessive autosomal genetic disorder Ataxia telangiectasia (A-T) is associated with DDR defects, endogenous OS and premature ageing. Here, we find frequent nuclear shape alterations in A-T cells, as well as accumulation of the key nuclear architecture component lamin B1. Lamin B1 overexpression is sufficient to induce nuclear shape alterations and senescence in wild-type cells, and normalizing lamin B1 levels in A-T cells reciprocally reduces both nuclear shape alterations and senescence. We further show that OS increases lamin B1 levels through p38 Mitogen Activated Protein kinase activation. Lamin B1 accumulation and nuclear shape alterations also occur during stress-induced senescence and oncogene-induced senescence (OIS), two canonical senescence situations. These data reveal lamin B1 as a general molecular mediator that controls OS-induced senescence, independent of established Ataxia Telangiectasia Mutated (ATM) roles in OIS.
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“Since then, several studies have confirmed the reduction of LMNB1 in various senescent cell types (Barascu et al. 2012; Freund et al. 2012; Dreesen et al. 2013; Sadaie et al. 2013; Shah et al. 2013).”
From Cellular senescence and its effector programs (2014) · cites this paper as Barascu et al. 2012
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“Other DNA lesions—such as those caused by oxidative stress—may also drive cells into senescence (35–38).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [35]
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“Oxidative stress has been ensured as a crucial factor for cellular senescence through shortening telomere and causing DNA double-strand breaks.209,210”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [209]
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“Compared with LMNB1 depletion, phenotypes induced by ectopic LMNB1 were more heterogeneous between studies: Overexpression of LMNB1 either delays (Shimi et al. 2011) or enhances senescence (Barascu et al. 2012; Dreesen et al. 2013) or exhibits a minimal effect on proliferation (Sadaie et al. 2013).”
From Cellular senescence and its effector programs (2014) · cites this paper as Barascu et al. 2012
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“Similarly, Barascu et al. (2012) showed that increased levels of LMNB1 are associated with ROS up-regulation and senescence.”
From Cellular senescence and its effector programs (2014) · cites this paper as Barascu et al. 2012
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“Oxidative stress has been ensured as a crucial factor for cellular senescence through shortening telomere and causing DNA double-strand breaks.(209,210) Moreover, infections,(211) environmental pollution,(212,213) and adverse lifestyle habits(214) can increase oxidative stress.”
BackgroundLamin B1 loss is a senescence-associated biomarker
Freund, A., Laberge, R.-M., Demaria, M., & Campisi, J. (2012) · Molecular Biology of the Cell · doi:10.1091/mbc.e11-10-0884 · Cited by 1,046
“A recent report (Barascu et al., 2012) showed that oxidative stress induces senescence via an increase in lamin B1 expres-”
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“Since then, several studies have confirmed the reduction of LMNB1 in various senescent cell types (Barascu et al. 2012; Freund et al. 2012; Dreesen et al. 2013; Sadaie et al. 2013; Shah et al. 2013).”
BackgroundInfluentialShah, P. P., Donahue, G., Otte, G. L., Capell, B. C., Nelson, D. M., Cao, K., Aggarwala, V., Cruickshanks, H. A., Rai, T. S., McBryan, T., et al. (2013) · Genes & Development · doi:10.1101/gad.223834.113 · Cited by 550
“We note that certain cell types and disease states exhibit opposite effects of lamin B1 alteration (Barascu et al. 2012; Dreesen et al. 2013).”
Background
Metadata
- Authors
- Barascu, A., Le Chalony, C., Pennarun, G., Genet, D., Imam, N., Lopez, B., & Bertrand, P.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- Corresponding author
- Bertrand, Pascale
- Venue
- The EMBO Journal
- Published
- 2012-01-13
- Volume
- 31
- Issue
- 5
- Pages
- 1080-1094
- ISSN
- 0261-4189 (ISSN-L)
- 1460-2075
- PMC
- PMC3297999
- OpenAlex
- W2160703969
- Cited by
- 206
- References
- 84
- Citations by year
- 2026: 6 · 2025: 14 · 2024: 12 · 2023: 8 · 2022: 11 · 2021: 16 · 2020: 17 · 2019: 9 · 2018: 12 · 2017: 12 · 2016: 17 · 2015: 15 · 2014: 24 · 2013: 15 · 2012: 18
- FWCI
- 9.25
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- The EMBO Journal (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- oxidative stress, cellular senescence, ATM, lamin B1, p38 MAPK, ataxia telangiectasia, DNA damage response, stress-induced senescence, oncogene-induced senescence, nuclear organization, premature aging
- MeSH terms
- Aging, Cells, Cultured, Humans, Signal Transduction, Oxidative Stress, Lamin Type B, p38 Mitogen-Activated Protein Kinases
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 ›
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