Evidence map›Paper›PMID 30728349›Full record

ArticleCell death & disease2019

p53 induces senescence through Lamin A/C stabilization-mediated nuclear deformation.

Min-Ho Yoon, So-Mi Kang, Su-Jin Lee, Tae-Gyun Woo, Ah-Young Oh, Soyoung Park, Nam-Chul Ha, Bum-Joon Park

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.5field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Mechanical Stress Triggers Premature Senescence in Cardiac Fibroblasts.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
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  11. Review
  12. Article
  13. Review
  14. Coaching ribosome biogenesis from the nuclear periphery.bioRxiv : the preprint server for biology · 2024
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Min-Ho YoonDepartment of Molecular Biology, College of Natural Science, Pusan National University, Busan, 46241, Republic of Korea.
So-Mi KangDepartment of Molecular Biology, College of Natural Science, Pusan National University, Busan, 46241, Republic of Korea.
Su-Jin LeeDepartment of Molecular Biology, College of Natural Science, Pusan National University, Busan, 46241, Republic of Korea.
Tae-Gyun WooDepartment of Molecular Biology, College of Natural Science, Pusan National University, Busan, 46241, Republic of Korea.
Ah-Young OhDepartment of Molecular Biology, College of Natural Science, Pusan National University, Busan, 46241, Republic of Korea.
Soyoung ParkDepartment of Molecular Biology, College of Natural Science, Pusan National University, Busan, 46241, Republic of Korea.
Nam-Chul HaDepartment of Food Science, College of Agricultural Science, Seoul National University, Seoul, 08826, Republic of Korea.ORCID http://orcid.org/0000-0003-4813-748X
Bum-Joon ParkDepartment of Molecular Biology, College of Natural Science, Pusan National University, Busan, 46241, Republic of Korea. bjpark1219@pusan.ac.kr.
Pusan National University · KRSeoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

p53-mediated cellular senescence has been intensively investigated, because it is important for tumor suppressive function. In addition, p16/INK4A is well known to be critical for cellular senescence. However, detailed molecular mechanism or relevance between p53 and p16-mediated senescence has not been demonstrated yet. Here we show that p53 induces p16 through Lamin A/C stabilization via direct interaction. Stabilized Lamin A/C promotes degradation of BMI-1 and MEL-18 (Polycomb repressor complex 1, PRC1), which sequesters p16 promotor. Increased p53 can reduce BMI-1/MEL-18 and induce p16 expression via Lamin A/C. Elimination of Lamin A/C can abolish p53-induced p16 expression and BMI-1/MEL-18 reduction. As Lamin A/C expression is increased during cell differentiation, this mechanism seems to be very useful for selective induction of senescence in non-stem cells. Our results suggest that Lamin A/C-p53 network is important for p16/INK4A-mediated cellular senescence.

Indexed as

Cell Line, TumorCell NucleusCellular SenescenceChildCyclin-Dependent Kinase Inhibitor p16DNA DamageFemaleFibroblastsGene Knockdown TechniquesHCT116 CellsHEK293 CellsHumansLaminsLamin Type AMitogen-Activated Protein Kinase 7Polycomb Repressive Complex 1CDKN2A protein, humanCyclin-Dependent Kinase Inhibitor p16lamin C protein, humanLaminsLamin Type ALMNA protein, humanMAPK7 protein, humanMitogen-Activated Protein Kinase 7PCGF2 protein, humanPolycomb Repressive Complex 1TP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID30728349
PMCPMC6365587
OpenAlexW2911928209

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.