Evidence map›Paper›PMID 39002537›Full record

ArticleDevelopmental cell2024

Shifts in keratin isoform expression activate motility signals during wound healing.

Benjamin A Nanes, Kushal Bhatt, Evgenia Azarova, Divya Rajendran, Sabahat Munawar, Tadamoto Isogai, Kevin M Dean, Gaudenz Danuser

Abstract read
In one paragraph

Article in Developmental cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Soluble CD83 Accelerates Wound Healing and Attenuates Inflammatory Responses Induced by Chronic Wound Fluid in a Human 3D in Vitro Wound Healing Model.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Benjamin A NanesDepartment of Dermatology, UT Southwestern Medical Center, Dallas, TX 75390, USA; Lyda Hill Department of Bioinformatics and Cecil H and Ida Green Center for Systems Biology, UT Southwestern Medical Center, Dallas, TX 75390, USA. Electronic address: benjamin.nanes@utsouthwestern.edu.
Kushal BhattLyda Hill Department of Bioinformatics and Cecil H and Ida Green Center for Systems Biology, UT Southwestern Medical Center, Dallas, TX 75390, USA.
Evgenia AzarovaLyda Hill Department of Bioinformatics and Cecil H and Ida Green Center for Systems Biology, UT Southwestern Medical Center, Dallas, TX 75390, USA.
Divya RajendranLyda Hill Department of Bioinformatics and Cecil H and Ida Green Center for Systems Biology, UT Southwestern Medical Center, Dallas, TX 75390, USA.
Sabahat MunawarLyda Hill Department of Bioinformatics and Cecil H and Ida Green Center for Systems Biology, UT Southwestern Medical Center, Dallas, TX 75390, USA.
Tadamoto IsogaiLyda Hill Department of Bioinformatics and Cecil H and Ida Green Center for Systems Biology, UT Southwestern Medical Center, Dallas, TX 75390, USA.
Kevin M DeanLyda Hill Department of Bioinformatics and Cecil H and Ida Green Center for Systems Biology, UT Southwestern Medical Center, Dallas, TX 75390, USA.
Gaudenz DanuserLyda Hill Department of Bioinformatics and Cecil H and Ida Green Center for Systems Biology, UT Southwestern Medical Center, Dallas, TX 75390, USA. Electronic address: gaudenz.danuser@utsouthwestern.edu.

Funding

UTSW-UNC Center for Cell Signaling AnalysisRM1GM145399 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI Kevin Michael Dean, Klaus M. Hahn · 2022 to 2026
$6.2M
Functional causality in regulating cell morphogenesisR35GM136428 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI DANUSER, GAUDENZ · 2020 to 2024
$4.1M
Dermatology Research Training ProgramT32AR065969 · NIAMS · UT SOUTHWESTERN MEDICAL CENTER · PI PONCIANO D CRUZ, Tamia Alisha Harris-Tryon · 2014 to 2026
$1.6M
TEM for UT Southwestern Electron Microscopy Core FacilityS10OD021685 · OD · UT SOUTHWESTERN MEDICAL CENTER · PI LUBY-PHELPS, KATHERINE J · 2017 to 2017
$398k
NIAMS NIH HHS T32 AR065969NIGMS NIH HHS R35 GM136428NIGMS NIH HHS RM1 GM145399NIH HHS S10 OD021685
6 · The paper itself

Abstract

Keratin intermediate filaments confer structural stability to epithelial tissues, but the reason this simple mechanical function requires a protein family with 54 isoforms is not understood. During skin wound healing, a shift in keratin isoform expression alters the composition of keratin filaments. If and how this change modulates cellular functions that support epidermal remodeling remains unclear. We report an unexpected effect of keratin isoform variation on kinase signal transduction. Increased expression of wound-associated keratin 6A, but not of steady-state keratin 5, potentiated keratinocyte migration and wound closure without compromising mechanical stability by activating myosin motors to increase contractile force generation. These results substantially expand the functional repertoire of intermediate filaments from their canonical role as mechanical scaffolds to include roles as isoform-tuned signaling scaffolds that organize signal transduction cascades in space and time to influence epithelial cell state.

Indexed as

Cell MovementKeratinocytesProtein IsoformsSignal TransductionWound HealingAnimalsHumansIntermediate FilamentsKeratinsMiceKeratinsProtein Isoformsintermediate filamentskeratinmyosinsignal transductionwound healing

Identifiers

PMID39002537
PMCPMC11496015

What OpenQuestion holds

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Registered trials

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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.