Evidence map›Paper›PMID 9298992›Full record

ArticleThe Journal of cell biology1997

Caspase cleavage of keratin 18 and reorganization of intermediate filaments during epithelial cell apoptosis.

C Caulín, G S Salvesen, R G Oshima

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 179 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
179citing papers in PubMed, 2 pooled it
11.5field-weighted citation impact, top 1% 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

179 citing papers in PubMed, 2 syntheses or guidelines pooled it, 592 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
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  6. Review
  7. Article
  8. In vitro liver models for toxicological research.Drug metabolism and pharmacokinetics · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Biomarkers of liver diseases.Molecular biology reports · 2023
    Review
  16. Article
  17. Article
  18. Apoptolysis: a less understood concept in the pathogenesis of Pemphigus Vulgaris.Apoptosis : an international journal on programmed cell death · 2022
    Review
  19. Article
  20. Review

119 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

C CaulínThe Burnham Institute (formerly the La Jolla Cancer Research Foundation), La Jolla, California 92037, USA.
G S Salvesen
R G Oshima
Sanford Burnham Prebys Medical Discovery Institute · US

Funding

Tumor Microenvironment and Cancer ImmunologyP30CA030199 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI Michael Jackson · 1985 to 2026
$107.2M
Using neuroeconomics to disentangle the transcriptional mechanisms underlying resilience versus susceptibility to stressR01MH051399 · NIMH · YALE UNIVERSITY · PI NESTLER, ERIC J. · 1994 to 2023
$10.2M
PROTEINASE INHIBITORY MECHANISMS OF SERPINSR01HL051399 · NHLBI · DUKE UNIVERSITY · PI SALVESEN, GUY S · 1995 to 2003
$1.8M
DEVELOPMENTAL CONTROL OF HUMAN CYTOKERATIN EXPRESSIONR01CA042302 · NCI · BURNHAM INSTITUTE FOR MEDICAL RESEARCH · PI OSHIMA, ROBERT G · 1986 to 2002
$1.4M
NCI NIH HHS 5 R01 CA42302NCI NIH HHS P30 CA030199NCI NIH HHS P30 CA30199NHLBI NIH HHS 5 R01 HL51399NIMH NIH HHS R01 MH051399
6 · The paper itself

Abstract

Keratins 8 (K8) and 18 (K18) are major components of intermediate filaments (IFs) of simple epithelial cells and tumors derived from such cells. Structural cell changes during apoptosis are mediated by proteases of the caspase family. During apoptosis, K18 IFs reorganize into granular structures enriched for K18 phosphorylated on serine 53. K18, but not K8, generates a proteolytic fragment during drug- and UV light-induced apoptosis; this fragment comigrates with K18 cleaved in vitro by caspase-6, -3, and -7. K18 is cleaved by caspase-6 into NH2-terminal, 26-kD and COOH-terminal, 22-kD fragments; caspase-3 and -7 additionally cleave the 22-kD fragment into a 19-kD fragment. The cleavage site common for the three caspases was the sequence VEVD/A, located in the conserved L1-2 linker region of K18. The additional site for caspases-3 and -7 that is not cleaved efficiently by caspase-6 is located in the COOH-terminal tail domain of K18. Expression of K18 with alanine instead of serine at position 53 demonstrated that cleavage during apoptosis does not require phosphorylation of serine 53. However, K18 with a glutamate instead of aspartate at position 238 was resistant to proteolysis during apoptosis. Furthermore, this cleavage site mutant appears to cause keratin filament reorganization in stably transfected clones. The identification of the L1-2 caspase cleavage site, and the conservation of the same or very similar sites in multiple other intermediate filament proteins, suggests that the processing of IFs during apoptosis may be initiated by a similar caspase cleavage.

Indexed as

CaspasesAdenocarcinomaAnimalsApoptosisCaspase 3Caspase 6Caspase 7Cysteine EndopeptidasesEndometrial NeoplasmsEnzyme PrecursorsEpitheliumFemaleGene ExpressionHumansIntermediate FilamentsKeratinsCASP3 protein, humanCasp3 protein, mouseCASP6 protein, humanCasp6 protein, mouseCASP7 protein, humanCasp7 protein, mouseCaspase 3Caspase 6Caspase 7CaspasesCysteine EndopeptidasesEnzyme PrecursorsKeratins

Identifiers

PMID9298992
PMCPMC2132555
OpenAlexW2049179639

What OpenQuestion 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 OpenQuestion graph.