The DOI matches its Crossref record; 83 of the 84 references it cites were found in a registry or an index.
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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1 retracted
WITHDRAWN: Oxidative stress in aging: Theoretical outcomes and clinical evidences in humans
del Valle, L. G. (2010) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2010.09.010 · Cited by 36
RetractedAging: a theory based on free radical and radiation chemistry
Harman, D. (1956) · Journal of Gerontology · doi:10.1093/geronj/11.3.298 · Cited by 8,567
A biomarker that identifies senescent human cells in culture and in aging skin in vivo.
Dimri, G. P., Lee, X., Basile, G., Acosta, M., Scott, G., Roskelley, C., Medrano, E. E., Linskens, M., Rubelj, I., & Pereira-Smith, O. (1995) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.92.20.9363 · Cited by 7,477
ATM and ATR Substrate Analysis Reveals Extensive Protein Networks Responsive to DNA Damage
Matsuoka, S., Ballif, B. A., Smogorzewska, A., McDonald, E. R., Hurov, K. E., Luo, J., Bakalarski, C. E., Zhao, Z., Solimini, N., Lerenthal, Y., et al. (2007) · Science · doi:10.1126/science.1140321 · Cited by 3,075
Direct observation of individual endogenous protein complexes in situ by proximity ligation
Söderberg, O., Gullberg, M., Jarvius, M., Ridderstråle, K., Leuchowius, K.-J., Jarvius, J., Wester, K., Hydbring, P., Bahram, F., Larsson, L.-G., et al. (2006) · Nature Methods · doi:10.1038/nmeth947 · Cited by 2,419
Persistent DNA damage signalling triggers senescence-associated inflammatory cytokine secretion
Rodier, F., Coppé, J.-P., Patil, C. K., Hoeijmakers, W. A. M., Muñoz, D. P., Raza, S. R., Freund, A., Campeau, E., Davalos, A. R., & Campisi, J. (2009) · Nature Cell Biology · doi:10.1038/ncb1909 · Cited by 2,232
Four faces of cellular senescence
Rodier, F., & Campisi, J. (2011) · Journal of Cell Biology · doi:10.1083/jcb.201009094 · Cited by 2,070 · cited 1×
“On the other hand, in contrast, beside its putative role in organism ageing, recent data have proposed that senescent cells could favour tumour proliferation or invasion by secreting inflammatory factors (Rodier et al , 2009; Campisi et al , 2011; Rodier and Campisi, 2011).”
Oncogene-induced senescence is part of the tumorigenesis barrier imposed by DNA damage checkpoints
Bartkova, J., Rezaei, N., Liontos, M., Karakaidos, P., Kletsas, D., Issaeva, N., Vassiliou, L.-V. F., Kolettas, E., Niforou, K., Zoumpourlis, V. C., et al. (2006) · Nature · doi:10.1038/nature05268 · Cited by 1,986
Oncogene-induced senescence is a DNA damage response triggered by DNA hyper-replication
Di Micco, R., Fumagalli, M., Cicalese, A., Piccinin, S., Gasparini, P., Luise, C., Schurra, C., Garre’, M., Giovanni Nuciforo, P., Bensimon, A., et al. (2006) · Nature · doi:10.1038/nature05327 · Cited by 1,821
Protein detection using proximity-dependent DNA ligation assays
Fredriksson, S., Gullberg, M. T., Jarvius, J., Olsson, C., Pietras, K., Gustafsdottir, S., Östman, A., & Landegren, U. D. (2002) · Nature Biotechnology · doi:10.1038/nbt0502-473 · Cited by 1,518
Cited by
Sorted by citations
Aging, Cellular Senescence, and Cancer
Campisi, J. (2013) · Annual Review of Physiology · doi:10.1146/annurev-physiol-030212-183653 · Cited by 2,954
Inflammation and aging: signaling pathways and intervention therapies
Li, X., Li, C., Zhang, W., Wang, Y., Qian, P., & Huang, H. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01502-8 · Cited by 1,443
“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-”
BackgroundCellular senescence and its effector programs
Salama, R., Sadaie, M., Hoare, M., & Narita, M. (2014) · Genes & Development · doi:10.1101/gad.235184.113 · Cited by 855
“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
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