Evidence map›Paper›PMID 36231039›Full record

ArticleCells2022

A Ca

Sonia Ratajczyk, Corinne Drexler, Reinhard Windoffer, Rudolf E Leube, Peter Fuchs

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 46% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. SRC and ERK Regulate the Turnover of Cytoskeletal Keratin Filaments.International journal of molecular sciences · 2025
    Article
  3. 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

5 authors at 2 institutions in 2 countries.

Sonia RatajczykMax Perutz Labs, Department of Biochemistry and Cell Biology, University of Vienna, Vienna Biocenter Campus (VBC), A-1030 Vienna, Austria.
Corinne DrexlerMax Perutz Labs, Department of Biochemistry and Cell Biology, University of Vienna, Vienna Biocenter Campus (VBC), A-1030 Vienna, Austria.
Reinhard WindofferInstitute of Molecular and Cellular Anatomy, RWTH Aachen University, Wendlingweg 2, 52074 Aachen, Germany.
Rudolf E LeubeInstitute of Molecular and Cellular Anatomy, RWTH Aachen University, Wendlingweg 2, 52074 Aachen, Germany.ORCID 0000-0002-5519-7379
Peter FuchsMax Perutz Labs, Department of Biochemistry and Cell Biology, University of Vienna, Vienna Biocenter Campus (VBC), A-1030 Vienna, Austria.ORCID 0000-0003-3933-7674
University of Vienna · ATRWTH Aachen University · DE

Funding

Austrian Science Fund FWF P 30310
6 · The paper itself

Abstract

Keratins exert important structural but also cytoprotective functions. They have to be adaptable to support cellular homeostasis. Epiplakin (EPPK1) has been shown to decorate keratin filaments in epithelial cells and to play a protective role under stress, but the mechanism is still unclear. Using live-cell imaging of epithelial cells expressing fluorescently tagged EPPK1 and keratin, we report here an unexpected dynamic behavior of EPPK1 upon stress. EPPK1 was diffusely distributed throughout the cytoplasm and not associated with keratin filaments in living cells under standard culture conditions. However, ER-, oxidative and UV-stress, as well as cell fixation, induced a rapid association of EPPK1 with keratin filaments. This re-localization of EPPK1 was reversible and dependent on the elevation of cytoplasmic Ca

Indexed as

CytoskeletonKeratinsAutoantigensIntermediate FilamentsAutoantigensepiplakinKeratinscytoskeletonepiplakinintermediate filamentskeratinplakin protein family

Identifiers

PMID36231039
PMCPMC9563781
OpenAlexW4303628229

What OpenQuestion holds

Textmetadata
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.