Evidence map›Paper›PMID 30133342›Full record

ArticleMolecular biology of the cell2018

Activation of the apoptotic pathway during prolonged prometaphase blocks daughter cell proliferation.

Yumi Uetake, Greenfield Sluder

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Cell confinement initiates a delayed but heritable loss of chromosomes.bioRxiv : the preprint server for biology · 2026
    Article
  5. When the Clock Is Ticking: The Role of Mitotic Duration in Cell Fate Determination.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  6. The two sides of chromosomal instability: drivers and brakes in cancer.Signal transduction and targeted therapy · 2024
    Review
  7. Permission to pass: on the role of p53 as a gatekeeper for aneuploidy.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2023
    Review
  8. Article
  9. Human centrosome organization and function in interphase and mitosis.Seminars in cell & developmental biology · 2021
    Review
  10. TransplantingAging · 2020
    Article
  11. Article
  12. Review
  13. Article
  14. 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

2 authors at 1 institution in 1 country.

Yumi UetakeDepartment of Radiology, University of Massachusetts Medical School, Worcester, MA 01655.
Greenfield SluderDepartment of Radiology, University of Massachusetts Medical School, Worcester, MA 01655.
University of Massachusetts Chan Medical School · US

Funding

RNA IN FORMATION, FUNCTION, AND REPRODUCTION OF CENTROSOR01GM030758 · NIGMS · WORCESTER FOUNDATION FOR BIOMEDICAL RES · PI SLUDER, GREENFIELD · 1985 to 2014
$6.4M
NIGMS NIH HHS R01 GM030758
6 · The paper itself

Abstract

When untransformed human cells spend >1.5 h in prometaphase under standard culture conditions, all daughters arrest in G1 despite normal division of their mothers. We investigate what happens during prolonged prometaphase that leads to daughter cell arrest in the absence of DNA damage. We find that progressive loss of anti-apoptotic MCL-1 activity and oxidative stress act in concert to partially activate the apoptosis pathway, resulting in the delayed death of some daughters and senescence for the rest. At physiological oxygen levels, longer prometaphase durations are needed for all daughters to arrest. Partial activation of apoptosis during prolonged prometaphase leads to persistent caspase activity, which activates the kinase cascade mediating the post-mitotic activation of p38. This in turn activates p53, and the consequent expression of p21stops the cell cycle. This mechanism can prevent cells suffering intractable mitotic defects, which modestly prolong mitosis but allow its completion without DNA damage, from producing future cell generations that are susceptible to the evolution of a transformed phenotype.

Indexed as

ApoptosisPrometaphaseCaspase InhibitorsCaspasesCell Cycle CheckpointsCell LineCell ProliferationCellular SenescenceEnzyme ActivationHumansMyeloid Cell Leukemia Sequence 1 ProteinOxidative StressOxygenp38 Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-bcl-2Caspase InhibitorsCaspasesMCL1 protein, humanMyeloid Cell Leukemia Sequence 1 ProteinOxygenp38 Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-bcl-2

Identifiers

PMID30133342
PMCPMC6249836
OpenAlexW2888484271

What Socratic holds

Textmetadata
LicenceCC BY-NC-SA
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 Socratic graph.