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Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type- and insult-dependent manner and follow expression of p16ink4a
Open accessAbstract
Cellular senescence, an irreversible proliferation arrest evoked by stresses such as oncogene activation, telomere dysfunction, or diverse genotoxic insults, has been implicated in tumor suppression and aging. Primary human fibroblasts undergoing oncogene-induced or replicative senescence are known to form senescence-associated heterochromatin foci (SAHF), nuclear DNA domains stained densely by DAPI and enriched for histone modifications including lysine9-trimethylated histone H3. While cellular senescence occurs also in premalignant human lesions, it is unclear how universal is SAHF formation among various cell types, under diverse stresses, and whether SAHF occur in vivo. Here, we report that human primary fibroblasts (BJ and MRC-5) and primary keratinocytes undergoing replicative senescence, or premature senescence induced by oncogenic H-Ras, diverse chemotherapeutics and bacterial cytolethal distending toxin, show differential capacity to form SAHF. Whereas all tested cell types formed SAHF in response to activated H-Ras, only MRC-5, but not BJ fibroblasts or keratinocytes, formed SAHF under senescence induced by etoposide, doxorubicin, hydroxyurea, bacterial intoxication or telomere attrition. In addition, DAPI-defined SAHF were detected on paraffin sections of Ras-transformed cultured fibroblasts, but not human lesions at various stages of tumorigenesis. Overall, our results indicate that unlike the widely present DNA damage response marker γH2AX, SAHF is not a common feature of cellular senescence. Whereas SAHF formation is shared by diverse cultured cell types under oncogenic stress, SAHF are cell-type-restricted under genotoxin-induced and replicative senescence. Furthermore, while the DNA/DAPI-defined SAHF formation in cultured cells parallels enhanced expression of p16(ink4a) , such 'prototypic' SAHF are not observed in tissues, including premalignant lesions, irrespective of enhanced p16(ink4a) and other features of cellular senescence.
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“Of note, the proportions of SAHF-positive cells did not change during extended periods of cultivation until 250 days after oncogene transduction.”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > SAHF formation is common in oncogene-induced senescence.
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In the paper
“In time course experiments, lentiviral transduction of H-Ras V12 led in all three cell types to widespread cellular senescence by day 12 after transduction, as judged by changes in morphology, enhanced SA-β-Gal staining (Fig. 1) and grossly diminished DNA replication indicated by inhibited incorporation of BrdU (Sup.Table 1).”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > SAHF formation is common in oncogene-induced senescence.
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“In contrast to BJ cells, and consistent with the degree of SAHF formation, extracts of MRC-5 cells undergoing senescence showed increased p16 ink4a in all six scenarios, albeit to different levels.”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > SAHF formation is common in oncogene-induced senescence.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn the paper
“Consistent with the data obtained on paraffin sections, no clear evidence of the classical DNA/DAPI-defined SAFH was seen upon examination of these adenoma frozen sections, despite the positive variable and partly even focal, expression pattern of the heterochromatin markers HP1γ, H3K9Me3 and SA-β-gal activity (data not shown and Sup.Material reviewed in ref. 48).”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > SAHF formation is common in oncogene-induced senescence.
What the sources say
- Not checked yetcites [48]
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In the paper
“the close correlation of the ability to form SAHF and the increased level of p16 ink4a”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > Discussion
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In the paper
“As can be seen from the examples of Ras-transformed BJ fibroblasts, immunohistochemical examination of paraffin sections still revealed the DNA/DAPI-defined SAHF in such specimens (Fig. 5A), albeit at somewhat lower frequency compared to senescent BJ cells grown and analyzed directly on coverslips (Fig. 1).”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > SAHF formation is common in oncogene-induced senescence.
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In the paper
“In contrast to sections from paraffin embedded Ras-transformed BJ cells, no SAHF formation was observed on tissue sections of normal epithelial tissues, adenomas or carcinomas (Fig. 5B and data not shown).”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > SAHF formation is common in oncogene-induced senescence.
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In the paper
“This differential SAHF formation was not altered even when the experiments were prolonged until day 21 of keratinocytes (Fig. 4A and C and data not shown)”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > SAHF formation is common in oncogene-induced senescence.
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In the paper
“we did find elevated γH2AX in all three cell types, and under senescence induced by all six stimuli studied here”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > Discussion
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In the paper
“Overall, the proportion of SAHF-positive cells among the drug-induced MRC-5 senescent cells was lower (approx.20%) than in oncogene-induced MRC-5 senescent cells, despite a similar overall senescent phenotype was seen in settings with distinct senescenceinducing stimuli (Figs. 2 and 3, Sup.Table 1 and Sup.Fig. 1).”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > SAHF formation is common in oncogene-induced senescence.
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- It may state two separate claims as one. 22
- The quote only partly states this claim. 1
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In the paper
“The first detectable SAHF appeared at day 5 in all three cell types, with the highest percentage of the initially positive cells seen in MRC-5 (Fig. 2A).”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > SAHF formation is common in oncogene-induced senescence.
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In the paper
“The initial differences in relative proportions of SAHF-positive cells among the three cell types became minimized by day 12, however, when no statistically significant differences in percentages of SAHFpositive cells were found (Fig. 2A).”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > SAHF formation is common in oncogene-induced senescence.
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
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In the paper
“Notably, the highest and lowest abundance of p16 ink4a were found in MRC-5 senescent after Ras and doxorubicin exposure, respectively (Fig. 6A).”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > SAHF formation is common in oncogene-induced senescence.
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
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In the paper
“In contrast to consistent heterochromatinization and SAHF formation during the Ras oncogene-induced senescence in all three cell types, drug-induced senescence was accompanied by SAHF formation only in MRC-5 cells, but not in BJ or keratinocytes treated with any of the three drugs (Figs. 2 and 3).”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > SAHF formation is common in oncogene-induced senescence.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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In the paper
“Specifically, in cell extracts of senescent BJ cells, robust induction of p16 ink4a was only apparent under Ras-induced senescence, the only condition associated with the occurrence of classical DNA/DAPI-defined SAHF in these cells.”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > SAHF formation is common in oncogene-induced senescence.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Whereas all tested cell types formed SAHF in response to activated H-Ras, only MRC-5, but not BJ fibroblasts or keratinocytes, formed SAHF under senescence induced by etoposide, doxorubicin, hydroxyurea, bacterial intoxication or telomere attrition.”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > Introduction
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In the paper
“Interestingly, the 'old,' senescent populations of MRC-5 cells displayed DAPI-stained DNA/SAHF foci accompanying other features of senescence in contrast to lack of SAHF formation in senescent BJ fibroblasts (Fig. 4B and D) despite the fact that both strains shared other recognized features of the senescent phenotype and the fact that the BJ cells reached the senescent state after more passages in”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > SAHF formation is common in oncogene-induced senescence.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“despite the fact that both strains shared other recognized features of the senescent phenotype and the fact that the BJ cells reached the senescent state after more passages in vitro compared to MRC-5.”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > SAHF formation is common in oncogene-induced senescence.
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
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In the paper
“Formation of DAPI-defined SAHF that colocalized with heterochromatin markers H3K9Me3 and HP1γ was observed in HdCDT-exposed senescent MRC-5 cells but not in similarly treated BJ cells and”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > SAHF formation is common in oncogene-induced senescence.
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In the paper
“functionally SAHF have been implicated in transcriptional silencing of proliferationpromoting genes.4”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > SAHF formation is common in oncogene-induced senescence.
What the sources say
- Not checked yetcites [4]
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“premature senescence induced by activated Ras oncogene, 22 bacterial intoxication 42 and several genotoxic chemotherapeutics”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > Introduction
What the sources say
- Not checked yetcites [22]
- Not checked yetcites [42]
Strength:boosted· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“First, our data strongly indicate that SAHF formation is not a universal component of the senescence program and, in fact, appears to be dispensable for multiple modes of cellular senescence, in various cell types.”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > SAHF formation is common in oncogene-induced senescence.
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In the paper
“We conclude that unlike the universal occurrence of SAHF in oncogene-induced senescence, SAHF formation is restricted to only one of the three normal human cell types undergoing senescence evoked by several genotoxic drugs.”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > SAHF formation is common in oncogene-induced senescence.
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In the paper
“γH2AX and other functional markers of activated DDR can conveniently be assessed on tissue sections.13,48,[53][54][55]”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > Discussion
What the sources say
- Not checked yetcites [13]
- Not checked yetcites [48]
- Not checked yetcites [53]
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Collectively, these experiments further support the notion that the ability to form SAHF does not necessarily correlate with the senescent state, here documented for replicative and toxinevoked senescence, and that the MRC-5 cells are more prone to SAHF formation compared to other normal cell types including epithelial cells.”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > SAHF formation is common in oncogene-induced senescence.
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In the paper
“a scenario that we recently reported to induce cellular senescence in the subpopulations of various human cell types, both normal and cancer-derived”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > SAHF formation is common in oncogene-induced senescence.
What the sources say
- Not checked yetcites [42]
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Furthermore, the data also show that unlike senescent, arrested cells, the proliferating cancer cells do not form the classical DNA/DAPIdefined SAHF, which are apparently distinct from the H3K9Me3/HP1γ-rich heterochromatin domains that do not necessarily reflect silencing of proliferation genes such as cyclin A, a protein highly expressed in all cell lines of our panel (data not shown).”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > SAHF formation is common in oncogene-induced senescence.
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In the paper
“We have previously reported that cellular senescence observed in clinical specimens of premalignant human lesions is accompanied by enhanced heterochromatinization markers H3K9Me3 and HP1γ that correlated with active DNA damage signaling.48”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > SAHF formation is common in oncogene-induced senescence.
What the sources say
- Not checked yetcites [48]
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Several chemotherapeutic drugs including etoposide, 43 hydroxyurea 44 and doxorubicin 45,46 are known to induce premature senescence in human cells.”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > SAHF formation is common in oncogene-induced senescence.
What the sources say
- Not checked yetcites [43]
- Not checked yetcites [44]
- Not checked yetcites [45]
- Not checked yetcites [46]
Strength:boosted· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Whereas SAHF formation is shared by diverse cultured cell types under oncogenic stress, SAHF are cell-type-restricted under genotoxin-induced and replicative senescence.”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > Introduction
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In the paper
“The diagnoses were independently verified by two experienced pathologists according to the established criteria of classification recommended by the World Health Organization.”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > Additional information
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In the paper
“Alpha-tubulin was used as a marker to ensure equal loading.”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > Additional information
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In the paper
“the p16 ink4a -mediated senescence-associated proliferation arrest appears to be more robust and irreversible even upon depletion of p53, as compared to the possibly partially reversible arrest under p16 ink4a -low conditions, at least in replicative senescence.32”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > Discussion
What the sources say
- Not checked yetcites [32]
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
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In the paper
“For quantitative and comparative imaging, identical image acquisition parameters were used.”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > Discussion
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In the paper
“All samples were originally collected at the University hospitals in Aarhus and Copenhagen, under ethical approval received from a local Medical Research Ethics Committee in Denmark.”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > Additional information
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In the paper
“The results shown are averages (with 95% confidence interval, tested by unpaired t-test) of a minimum of three independent experiments.”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > Data analysis and statistics.
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The overall picture emerging is that p16 ink4a , albeit not essential for every mode of cellular senescence, is critical for the formation of SAHF, 4 robust engagement of pRb and irreversible cell cycle arrest, 62,63”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > Discussion
What the sources say
- Not checked yetcites [4]
- Not checked yetcites [62]
- Not checked yetcites [63]
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“It appears that in cells with low expression of p16 ink4a , senescence induction relies more on the p53-p21 axis, and possibly other mechanisms, likely including also DNA damage checkpoints, only some of which require p53.”
§ Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type-and insult-dependent manner and follow expression of p16 ink4a > Discussion
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
The paper relies on this without support.
p16ink4a protein abundance reflects activation of the p16ink4a-pRb pathway in the cells studied.
“we argued that the observed differences might reflect variable levels of the p16 ink4a CDK inhibitor, and hence the activation of the pRb pathway, whose role in SAHF formation has been documented.4,38”
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?
In the citing paper
“At the same time, p16 induction is robust in response to oncogenic stimuli, even in cells that undergo replicative senescence with low p16 levels [52].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [52]
In the citing paper
“However, SAHF formation is not a universal feature of senescence.”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [52]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
The bacterial-intoxication citation points to a drug study
MinorReference 42 is cited for a previously described mode of senescence induced by bacterial intoxication, but its listed article concerns DNA-damage-induced senescence in tumor cells.
“the most recently described senescence mode induced by bacterial intoxication, 42”
“42. te Poele RH, Okorokov AL, Jardine L, Cummings J, Joel SP. DNA damage is able to induce senescence in tumor cells in vitro and in vivo. Cancer Res 2002; 62:1876-83.”
Error bars are described as both confidence intervals and standard deviations
MinorThe statistics section says the results are shown with 95% confidence intervals, but the Figure 2 legend says its error bars show standard deviations. These are different measures of variability.
“The results shown are averages (with 95% confidence interval, tested by unpaired t-test) of a minimum of three independent experiments.”
“error bars represent the SD of three separate experiments.”
Holotoxin-preparation citations do not match the listed papers
MinorThe methods attribute preparation of the bacterial toxin subunits and holotoxin to references 47 and 75. The listed entries concern a tumorigenesis barrier and H2AX phosphorylation, respectively, rather than that preparation.
“Preparation of CdtA, CdtB and CdtC subunits and reconstitution of the active holotoxin (HdCDT) was previously described in references 47 and 75.”
“47. Bartkova J, Rezaei N, Liontos M, Karakaidos P, Kletsas D, Issaeva N, et al. Oncogene-induced senescence is part of the tumorigenesis barrier imposed by DNA damage checkpoints. Nature 2006; 444:633-7.”
Reference 48 does not match the cited earlier study
MinorThe text attributes an earlier study of heterochromatin markers in premalignant lesions to reference 48. The listed reference 48 is instead a study of BMI-1026-induced SAHF formation by different authors.
“We have previously reported that cellular senescence observed in clinical specimens of premalignant human lesions is accompanied by enhanced heterochromatinization markers H3K9Me3 and HP1γ that correlated with active DNA damage signaling.48”
“48. Seo HJ, Park HJ, Choi HS, Hwang SY, Park JS, Seong YS. BMI-1026 treatment can induce SAHF formation by activation of Erk1/2. BMB Rep 2008; 41:523-8.”
Citations
Cites
A biomarker that identifies senescent human cells in culture and in aging skin in vivo.
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Small Changes, Big Effects: Chromatin Goes Aging
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Ho, C. Z., Deng, L., Picone, R., Abderazzaq, F. O., Flanagan, N., Chua, D. Z., Low, B. C., & Wu, S. K. (2025) · Molecular Biology of the Cell · doi:10.1091/mbc.e24-10-0445 · Cited by 5
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Du, T., Liu, N., Zhang, W., Shi, H., & Zhang, T. (2017) · Europe PMC (PubMed Central) · doi:10.3969/j.issn.1673-4254.2017.03.14 · Cited by 5
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Mosaic Regulation of Stress Pathways Underlies Senescent Cell HeterogeneityPreprint
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Targeting telomere dynamics with plant-derived compounds: Molecular strategies against aging
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Gupta, K. P., Dholaniya, P. S., Chekuri, A., & Kondapi, A. K. (2015) · AGE · doi:10.1007/s11357-015-9810-0 · Cited by 4
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Laboratory Techniques in Cellular and Molecular Medicine
Ed., J. S., Janošťáková, A., Das, V., Kudlová, N., Stránská, J., Buriánová, R., Kotulová, J., Schadich, E., Ondra, M., Kubíčková, A., et al. (2022) · doi:10.5507/lf.22.24460499 · Cited by 5
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Cellular Senescence and Tumor Promotion
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Bi, J., Zeng, J., Liu, X., Mo, C., Yao, M., Zhang, J., Yuan, P., Jia, B., & Xu, S. (2024) · Saudi Pharmaceutical Journal · doi:10.1016/j.jsps.2024.102209 · Cited by 2
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Senescence in Aging, Within the Brain and Other Diseases: Mechanisms and Interventions
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Methods to Study MYC-Regulated Cellular Senescence
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Epigenetic Disordering Drives Stemness, Senescence Escape and Tumor HeterogeneityPreprint
Magnani, E., Macchi, F., Randic, T., Chen, C., Madakashira, B. P., Ranjan, S., Eski, S. E., Singh, S. P., & Sadler, K. C. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.12.29.629346 · Cited by 2
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Genetic and Epigenetic Influences on Cutaneous Cellular Senescence
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The Role of Sirtuins in Cellular Senescence and the Development of Age-Associated Diseases
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Pharmacologic Inhibition of Cardiac Stem Cell Senescence
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Cellular Senescence and Its Relation with Telomere
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Burrow, K. L. (2014) · Research Explorer (The University of Manchester) · Cited by 1
Premalignancy and Cellular Senescence
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The primary cilium as a regulator of cellular senescence in human fibroblasts
Breslin, L. (2014) · ARAN (University of Galway Research Repository) (Ollscoil na Gaillimhe – University of Galway) · doi:10.13025/17764
The effect of radiation on cellular ageing
Sabin, R. J. (2012) · Brunel University Research Archive (BURA) (Brunel University London)
The Regulation of Satellite Cell Function and Myogenesis by Isoforms of C/EBPβ
Lee, H. (2015) · uO Research (University of Ottawa) · doi:10.20381/ruor-4173
Effect of Polysaccharides from Angelica and Astragalus on Delaying WI-38 Cellular Senescence
Pu, X., Liu, L., Ma, X., Ren, J., Li, X., Li, H., & Yu, S. (2016) · International Conference on Medicine and Biopharmaceutical · doi:10.1142/9789814719810_0099
Johmura, Y., & Nakanishi, M. (2016) · Springer eBooks · doi:10.1007/978-4-431-55873-6_18
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ZNF313 is a novel cell cycle activator with an E3 ligase activity inhibiting cellular senescence by
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Senescence Markers: One is not Good Enough, We Need More!
Pk, S. (2016) · Open Access Journal of Microbiology & Biotechnology · doi:10.23880/oajmb-16000108
Cellular Senescence and Tumor Promotion
Demaria, M. (2017) · Springer eBooks · doi:10.1007/978-3-319-44870-1_79-1
The Molecular Physiology of Ageing: New Targets for Regenerative Medicine
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Purohit, J. S., Singh, N., Hussain, S. S., & Chaturvedi, M. M. (2020) · Springer eBooks · doi:10.1007/978-981-32-9005-1_9 · Cited by 1
γ- and δ-Tocotrienols interfere with senescence leading to decreased viability of cells
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Hoey, C. (2018) · TSpace (University of Toronto)
Stem cells and multiomics approaches in senescence: From benchside to bedside
Bişgin, A. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-820071-1.00015-3
Pathway Profiling Of Replicative And Induced Senescence
Purcell, M. (2014) · Human Biology
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Biological Functions of STAT, HP1, and Heterochromatin
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Celebrating 25 years of unraveling the mysteries of the cell cycle: a silver jubilee of cell biology
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Rôle de la kinase Akt dans la chimiorésistance : Régulation de l’équilibre Apoptose-Sénescence
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Generation of antisense RNAs at convergent gene loci in cells undergoing senescence
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Metadata
- Authors
- Kosar, M., Bartkova, J., Hubackova, S., Hodny, Z., Lukas, J., & Bartek, J.
- Affiliations
- Danish Cancer Society (DK)
- Venue
- Cell Cycle
- Publisher
- Informa UK Limited
- Published
- 2011-02
- Volume
- 10
- Issue
- 3
- Pages
- 457-468
- ISSN
- 1538-4101 (ISSN-L)
- 1551-4005
- OpenAlex
- W2083176422
- Semantic Scholar
- 815d4c31d4f348034a5d35051dd2bd5e4c9b9f36
- Cited by
- 283
- References
- 61
- Citations by year
- 2026: 4 · 2025: 8 · 2024: 8 · 2023: 14 · 2022: 13 · 2021: 20 · 2020: 17 · 2019: 15 · 2018: 17 · 2017: 21 · 2016: 29 · 2015: 27 · 2014: 23 · 2013: 30 · 2012: 27
- FWCI
- 19.63
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cell Cycle (publishedVersion)
- PubMed (publishedVersion)
- ASEP (submittedVersion, public-domain)
- Zenodo (CERN European Organization for Nuclear Research) (submittedVersion, other-oa)
- Funders
- European Commission
- National Research Foundation
- Danmarks Grundforskningsfond
- Grantová Agentura České Republiky (GAP301/10/1525, AV 0Z5039906, GA301/08/0353)
- Novo Nordisk
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- cellular senescence, senescence-associated heterochromatin foci, replicative senescence, oncogene-induced senescence, p16INK4a, genotoxic stress, telomere shortening, cytolethal distending toxin, keratinocytes, fibroblasts, precancerous lesions, histone H3K9 trimethylation, tumor suppression
- MeSH terms
- Bacterial Toxins, Cell Line, DNA Damage, Heterochromatin, Humans, Genes, ras, Cellular Senescence, Cyclin-Dependent Kinase Inhibitor p16, Cell Proliferation
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