Evidence map›Paper›PMID 9508776›Full record

ArticleThe Journal of cell biology1998

Lessons from keratin 18 knockout mice: formation of novel keratin filaments, secondary loss of keratin 7 and accumulation of liver-specific keratin 8-positive aggregates.

T M Magin, R Schröder, S Leitgeb, F Wanninger, K Zatloukal, C Grund, D W Melton

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
5.7field-weighted citation impact, top 4% 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

74 citing papers in PubMed, 207 citations in OpenAlex.

  1. Article
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  8. Article
  9. Article
  10. Keratin 8/18 Regulate the Akt Signaling Pathway.International journal of molecular sciences · 2021
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  12. Review
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  14. Article
  15. Article
  16. Review
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  18. Review
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  20. Article

14 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

7 authors at 3 institutions in 3 countries.

T M MaginInstitut fuer Genetik, Abteilung Molekulargenetik, Universitat Bonn, Bonn, Germany. t.magin@uni-bonn.de
R Schröder
S Leitgeb
F Wanninger
K Zatloukal
C Grund
D W Melton
German Cancer Research Center · DEUniversity of Edinburgh · GBDKFZ-ZMBH Alliance · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Here, we report on the analysis of keratin 18 null mice. Unlike the ablation of K8, which together with K18 is expressed in embryonic and simple adult epithelia, K18 null mice are viable, fertile, and show a normal lifespan. In young K18 null mice, hepatocytes were completely devoid of keratin filaments. Nevertheless, typical desmosomes were formed and maintained. Old K18 null mice, however, developed a distinctive liver pathology with abnormal hepatocytes containing K8-positive aggregates. These stained positively for ubiquitin and MM120-1 and were identified as Mallory bodies, one hallmark of human alcoholic hepatitis. This is the first demonstration that the ablation of one keratin leads to the accumulation of its single partner. Another striking finding was the absence or drastic down regulation of K7 in several tissues despite its ongoing transcription. Moreover, K18 null mice revealed new insights in the filament-forming capacity of the tail-less K19 in vivo. Due to the unexpected secondary loss of K7, only K8/19 are expressed in the uterine epithelium of K18 null mice. Immunoelectron microscopy of this tissue demonstrated the presence of typical K8/19 IF, thus highlighting in vivo that K19 is a fully competent partner for K8.

Indexed as

Age FactorsAnimalsAntibodies, MonoclonalDesmosomesEpithelial CellsFertilityGene ExpressionHeterozygoteHomozygoteIntermediate FilamentsKeratin-7KeratinsLife ExpectancyLiverMiceMice, KnockoutAntibodies, MonoclonalKeratin-7KeratinsKRT7 protein, humanKrt7 protein, mouseRNA, Messenger

Identifiers

PMID9508776
PMCPMC2132680
OpenAlexW1976347030

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.