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The NuA4 acetyltransferase and non-canonical chromatin-associated MRN/ATM activity temporally define senescence-associated secretory programs
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1 of the 78 references listed on this page is in the Retraction Watch database as retracted (export 2026-11-04): 10.1038/nature12201 (notice 2019-04-11).
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What this work says
Outgoing claims: the papers this work cites, builds on, or argues with.
inferredcites →https://doi.org/10.1007/978-1-62703-239-1_10openalex-snapshot
Detection of the Senescence-Associated Secretory Phenotype (SASP)
inferredcites →https://doi.org/10.1007/s10522-015-9593-9openalex-snapshot
Premature aging/senescence in cancer cells facing therapy: good or bad?
inferredcites →https://doi.org/10.1016/j.canlet.2012.01.007openalex-snapshot
DNA damage-induced cell death: From specific DNA lesions to the DNA damage response and apoptosis
inferredcites →https://doi.org/10.1016/j.cell.2008.03.038openalex-snapshot
Chemokine Signaling via the CXCR2 Receptor Reinforces Senescence
inferredcites →https://doi.org/10.1016/j.cell.2008.03.039openalex-snapshot
Oncogene-Induced Senescence Relayed by an Interleukin-Dependent Inflammatory Network
inferredcites →https://doi.org/10.1016/j.cell.2012.12.010openalex-snapshot
Monitoring Tumorigenesis and Senescence In Vivo with a p16INK4a-Luciferase Model
inferredcites →https://doi.org/10.1016/j.cell.2013.10.019openalex-snapshot
Programmed Cell Senescence during Mammalian Embryonic Development
inferredcites →https://doi.org/10.1016/j.cell.2013.10.041openalex-snapshot
Senescence Is a Developmental Mechanism that Contributes to Embryonic Growth and Patterning
inferredcites →https://doi.org/10.1016/j.cellsig.2010.03.017openalex-snapshot
Posttranslational modifications of NF-κB: Another layer of regulation for NF-κB signaling pathway
inferredcites →https://doi.org/10.1016/j.cellsig.2011.12.006openalex-snapshot
Emerging role of NF-κB signaling in the induction of senescence-associated secretory phenotype (SASP)
inferredcites →https://doi.org/10.1016/j.devcel.2014.11.012openalex-snapshot
An Essential Role for Senescent Cells in Optimal Wound Healing through Secretion of PDGF-AA
inferredcites →https://doi.org/10.1016/j.exger.2006.12.003openalex-snapshot
Accelerated immune senescence and HIV-1 infection
inferredcites →https://doi.org/10.1016/j.exger.2016.05.010openalex-snapshot
Keeping the senescence secretome under control: Molecular reins on the senescence-associated secretory phenotype
inferredcites →https://doi.org/10.1016/j.tcb.2006.07.007openalex-snapshot
Tip60 in DNA damage response and growth control: many tricks in one HAT
inferredcites →https://doi.org/10.1016/j.tcb.2017.07.004openalex-snapshot
Spatial and Temporal Control of Senescence
inferredcites →https://doi.org/10.1016/j.tibs.2016.05.008openalex-snapshot
The Metabolic Impact on Histone Acetylation and Transcription in Ageing
inferredcites →https://doi.org/10.1016/j.yexcr.2004.01.017openalex-snapshot
Histone deacetylase inhibitors induce a senescence-like state in human cells by a p16-dependent mechanism that is independent of a mitotic clock
inferredcites →https://doi.org/10.1016/s0092-8674(00)81902-9openalex-snapshot
Oncogenic ras Provokes Premature Cell Senescence Associated with Accumulation of p53 and p16INK4a
inferredcites →https://doi.org/10.1016/s0092-8674(03)00401-xopenalex-snapshot
Rb-Mediated Heterochromatin Formation and Silencing of E2F Target Genes during Cellular Senescence
inferredcites →https://doi.org/10.1016/s1097-2765(04)00256-4openalex-snapshot
Telomere Shortening Triggers Senescence of Human Cells through a Pathway Involving ATM, p53, and p21CIP1, but Not p16INK4a
inferredcites →https://doi.org/10.1038/emboj.2011.69openalex-snapshot
p38MAPK is a novel DNA damage response‐independent regulator of the senescence‐associated secretory phenotype
inferredcites →https://doi.org/10.1038/nature01368openalex-snapshot
DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation
inferredcites →https://doi.org/10.1038/nature02118openalex-snapshot
A DNA damage checkpoint response in telomere-initiated senescence
inferredcites →https://doi.org/10.1038/nature05077openalex-snapshot
The pathological response to DNA damage does not contribute to p53-mediated tumour suppression
inferredcites →https://doi.org/10.1038/nature10600openalex-snapshot
Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders
inferredcites →https://doi.org/10.1038/nature12201openalex-snapshot
KAT5 tyrosine phosphorylation couples chromatin sensing to ATM signalling
inferredcites →https://doi.org/10.1038/nature13193openalex-snapshot
The role of senescent cells in ageing
inferredcites →https://doi.org/10.1038/nature16932openalex-snapshot
Naturally occurring p16Ink4a-positive cells shorten healthy lifespan
inferredcites →https://doi.org/10.1038/nature25167openalex-snapshot
Senescence-associated reprogramming promotes cancer stemness
inferredcites →https://doi.org/10.1038/ncb1909openalex-snapshot
Persistent DNA damage signalling triggers senescence-associated inflammatory cytokine secretion
inferredcites →https://doi.org/10.1038/ncb1982openalex-snapshot
Histone H3 methylation links DNA damage detection to activation of the tumour suppressor Tip60
inferredcites →https://doi.org/10.1038/ncb2201openalex-snapshot
53BP1 nuclear bodies form around DNA lesions generated by mitotic transmission of chromosomes under replication stress
inferredcites →https://doi.org/10.1038/ncb2466openalex-snapshot
Telomeric DNA damage is irreparable and causes persistent DNA-damage-response activation
inferredcites →https://doi.org/10.1038/ncb2784openalex-snapshot
A complex secretory program orchestrated by the inflammasome controls paracrine senescence
inferredcites →https://doi.org/10.1038/ncb3195openalex-snapshot
MTOR regulates the pro-tumorigenic senescence-associated secretory phenotype by promoting IL1A translation
inferredcites →https://doi.org/10.1038/ncb3225openalex-snapshot
mTOR regulates MAPKAPK2 translation to control the senescence-associated secretory phenotype
inferredcites →https://doi.org/10.1038/ncb3397openalex-snapshot
NOTCH1 mediates a switch between two distinct secretomes during senescence
inferredcites →https://doi.org/10.1038/ncomms1708openalex-snapshot
Telomeres are favoured targets of a persistent DNA damage response in ageing and stress-induced senescence
inferredcites →https://doi.org/10.1038/ng1572openalex-snapshot
Temporal dissection of p53 function in vitro and in vivo
inferredcites →https://doi.org/10.1038/nm.4010openalex-snapshot
Clearance of senescent cells by ABT263 rejuvenates aged hematopoietic stem cells in mice
inferredcites →https://doi.org/10.1038/nm.4324openalex-snapshot
Local clearance of senescent cells attenuates the development of post-traumatic osteoarthritis and creates a pro-regenerative environment
inferredcites →https://doi.org/10.1038/nn.3715openalex-snapshot
Aberrant topoisomerase-1 DNA lesions are pathogenic in neurodegenerative genome instability syndromes
inferredcites →https://doi.org/10.1038/nrm3546openalex-snapshot
The ATM protein kinase: regulating the cellular response to genotoxic stress, and more
inferredcites →https://doi.org/10.1038/s41467-017-00314-zopenalex-snapshot
Identification of HSP90 inhibitors as a novel class of senolytics
inferredcites →https://doi.org/10.1042/bj20091329openalex-snapshot
Physical interaction between the histone acetyl transferase Tip60 and the DNA double-strand breaks sensor MRN complex
inferredcites →https://doi.org/10.1073/pnas.0905299106openalex-snapshot
Cell surface-bound IL-1α is an upstream regulator of the senescence-associated IL-6/IL-8 cytokine network
inferredcites →https://doi.org/10.1073/pnas.211053698openalex-snapshot
Senescent fibroblasts promote epithelial cell growth and tumorigenesis: A link between cancer and aging
inferredcites →https://doi.org/10.1073/pnas.92.10.4337openalex-snapshot
Oxidative DNA damage and senescence of human diploid fibroblast cells.
inferredcites →https://doi.org/10.1073/pnas.92.20.9363openalex-snapshot
A biomarker that identifies senescent human cells in culture and in aging skin in vivo.
inferredcites →https://doi.org/10.1074/jbc.m111.257071openalex-snapshot
Tumor Suppressor and Aging Biomarker p16INK4a Induces Cellular Senescence without the Associated Inflammatory Secretory Phenotype
inferredcites →https://doi.org/10.1074/jbc.m111.278465openalex-snapshot
New Molecular Bridge between RelA/p65 and NF-κB Target Genes via Histone Acetyltransferase TIP60 Cofactor
inferredcites →https://doi.org/10.1083/jcb.201009094openalex-snapshot
Four faces of cellular senescence
inferredcites →https://doi.org/10.1083/jcb.201305155openalex-snapshot
Probing the depths of cellular senescence
inferredcites →https://doi.org/10.1093/emboj/cdf660openalex-snapshot
Acetylation of RelA at discrete sites regulates distinct nuclear functions of NF‐κB
inferredcites →https://doi.org/10.1093/emboj/cdg417openalex-snapshot
Reversal of human cellular senescence: roles of the p53 and p16 pathways
inferredcites →https://doi.org/10.1093/jn/133.7.2485sopenalex-snapshot
Inhibition of Histone Deacetylase Activity by Butyrate
inferredcites →https://doi.org/10.1101/gad.223834.113openalex-snapshot
Lamin B1 depletion in senescent cells triggers large-scale changes in gene expression and the chromatin landscape
inferredcites →https://doi.org/10.1101/gad.227512.113openalex-snapshot
Cell fusion induced by ERVWE1 or measles virus causes cellular senescence
inferredcites →https://doi.org/10.1111/acel.12344openalex-snapshot
The Achilles’ heel of senescent cells: from transcriptome to senolytic drugs
inferredcites →https://doi.org/10.1126/science.1122446openalex-snapshot
Cellular Senescence in Aging Primates
inferredcites →https://doi.org/10.1126/science.1159051openalex-snapshot
Activation of the Cellular DNA Damage Response in the Absence of DNA Lesions
inferredcites →https://doi.org/10.1126/science.aaa5612openalex-snapshot
The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4
inferredcites →https://doi.org/10.1128/mcb.16.9.5210openalex-snapshot
Human Fibroblast Commitment to a Senescence-Like State in Response to Histone Deacetylase Inhibitors Is Cell Cycle Dependent
inferredcites →https://doi.org/10.1128/mcb.26.2.402-412.2006openalex-snapshot
The Transcriptional Histone Acetyltransferase Cofactor TRRAP Associates with the MRN Repair Complex and Plays a Role in DNA Double-Strand Break Repair
inferredcites →https://doi.org/10.1158/0008-5472.can-06-3985openalex-snapshot
Histone Deacetylase Inhibitors Synergize p300 Autoacetylation that Regulates Its Transactivation Activity and Complex Formation
inferredcites →https://doi.org/10.1158/0008-5472.can-11-3386openalex-snapshot
Chromatin Remodeling Underlies the Senescence-Associated Secretory Phenotype of Tumor Stromal Fibroblasts That Supports Cancer Progression
inferredcites →https://doi.org/10.1158/2159-8290.cd-13-0743openalex-snapshot
p38MAPK Plays a Crucial Role in Stromal-Mediated Tumorigenesis
inferredcites →https://doi.org/10.1158/2159-8290.cd-16-0241openalex-snapshot
Cellular Senescence Promotes Adverse Effects of Chemotherapy and Cancer Relapse
inferredcites →https://doi.org/10.1172/jci69738openalex-snapshot
New and emerging HDAC inhibitors for cancer treatment
inferredcites →https://doi.org/10.1242/jcs.01635openalex-snapshot
Stromal-epithelial interactions in aging and cancer: senescent fibroblasts alter epithelial cell differentiation
inferredcites →https://doi.org/10.1242/jcs.071340openalex-snapshot
DNA-SCARS: distinct nuclear structures that sustain damage-induced senescence growth arrest and inflammatory cytokine secretion
inferredcites →https://doi.org/10.1371/journal.pbio.0060301openalex-snapshot
Senescence-Associated Secretory Phenotypes Reveal Cell-Nonautonomous Functions of Oncogenic RAS and the p53 Tumor Suppressor
inferredcites →https://doi.org/10.1371/journal.pgen.1001354openalex-snapshot
H3 Lysine 4 Is Acetylated at Active Gene Promoters and Is Regulated by H3 Lysine 4 Methylation
inferredcites →https://doi.org/10.1371/journal.pone.0006529openalex-snapshot
A Versatile Viral System for Expression and Depletion of Proteins in Mammalian Cells
inferredcites →https://doi.org/10.18632/aging.101202openalex-snapshot
New agents that target senescent cells: the flavone, fisetin, and the BCL-XL inhibitors, A1331852 and A1155463
inferredcites →https://doi.org/10.3389/fgene.2015.00094openalex-snapshot
DDR-mediated crosstalk between DNA-damaged cells and their microenvironment
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