Evidence map›Paper›PMID 22942770›Full record

ArticleInternational journal of molecular sciences2012

The apoptotic volume decrease is an upstream event of MAP kinase activation during Staurosporine-induced apoptosis in HeLa cells.

Yuichi Hasegawa, Takahiro Shimizu, Nobuyuki Takahashi, Yasunobu Okada

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

17 citing papers in PubMed, 32 citations in OpenAlex.

  1. Hyperactive Rac converts sublethal to lethal trogocytosis in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Hyperactive Rac converts sublethal nibbling to lethal phagocytosisbioRxiv : the preprint server for biology · 2025
    Article
  3. A time window for rescuing dying retinal ganglion cells.Cell communication and signaling : CCS · 2024
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Inhibition of p38 mitogen-activated protein kinase phosphorylation decreases H₂O₂-induced apoptosis in human lens epithelial cells.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2015
    Article
  16. Article
  17. 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

4 authors at 1 institution in 1 country.

Yuichi HasegawaDepartment of Cell Physiology, National Institute for Physiological Sciences, Okazaki 444-8585, Japan.
Takahiro ShimizuDepartment of Cell Physiology, National Institute for Physiological Sciences, Okazaki 444-8585, Japan.
Nobuyuki TakahashiDepartment of Cell Physiology, National Institute for Physiological Sciences, Okazaki 444-8585, Japan.
Yasunobu OkadaDepartment of Cell Physiology, National Institute for Physiological Sciences, Okazaki 444-8585, Japan.
National Institute for Physiological Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Persistent cell shrinkage, called apoptotic volume decrease (AVD), is a pivotal event of apoptosis. Activation of the volume-sensitive outwardly rectifying Cl(-) channel (VSOR) is involved in the AVD induction. On the other hand, activation of the MAP kinase (MAPK) cascade is also known to play a critical role in apoptosis. In the present study, we investigated the relationship between the AVD induction and the stress-responsive MAPK cascade activation during the apoptosis process induced by staurosporine (STS) in HeLa cells. STS was found to induce AVD within 2-5 min and phosphorylation of c-Jun N-terminal kinase (JNK) and p38 MAPK after over 20-30 min. VSOR blockers suppressed not only STS-induced AVD but also phosphorylation of JNK and p38 as well as activation of caspase-3/7. Moreover, a p38 inhibitor, SB203580, and a JNK inhibitor, SP600125, failed to affect STS-induced AVD, whereas these compounds reduced STS-induced activation of caspase-3/7. Also, treatment with ASK1-specific siRNA suppressed STS-induced caspase-3/7 activation without affecting the AVD induction. Furthermore, sustained osmotic cell shrinkage per se was found to trigger phosphorylation of JNK and p38, caspase activation, and cell death. Thus, it is suggested that activation of p38 and JNK is a downstream event of AVD for the STS-induced apoptosis of HeLa cells.

Indexed as

AnthracenesApoptosisCaspase 3Caspase 7Cell SizeEnzyme ActivationEnzyme InhibitorsHeLa CellsHumansImidazolesMAP Kinase Kinase 4MAP Kinase Signaling Systemp38 Mitogen-Activated Protein KinasesPyridinesStaurosporineAnthracenesCASP3 protein, humanCASP7 protein, humanCaspase 3Caspase 7Enzyme InhibitorsImidazolesMAP Kinase Kinase 4p38 Mitogen-Activated Protein KinasespyrazolanthronePyridinesSB 203580Staurosporineanion channelapoptosisMAP kinaseshrinkagevolume regulation

Identifiers

PMID22942770
PMCPMC3430301
OpenAlexW2144849342

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.