Evidence map›Paper›PMID 38162019›Full record

ArticleiScience2023

A desmosomal cadherin controls multipotent hair follicle stem cell quiescence and orchestrates regeneration through adhesion signaling.

William V J Hariton, Katja Schulze, Siavash Rahimi, Taravat Shojaeian, Laurence Feldmeyer, Roman Schwob, Andrew M Overmiller, Beyza S Sayar, Luca Borradori, Mỹ G Mahoney and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in iScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. 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

12 authors at 3 institutions in 2 countries.

William V J HaritonDepartment of Dermatology, Inselspital, Bern University Hospital, University of Bern, 3010 Bern, Switzerland.
Katja SchulzeDermFocus, Vetsuisse Faculty, University of Bern, 3008 Bern, Switzerland.
Siavash RahimiDepartment of Dermatology, Inselspital, Bern University Hospital, University of Bern, 3010 Bern, Switzerland.
Taravat ShojaeianDepartment of Dermatology, Inselspital, Bern University Hospital, University of Bern, 3010 Bern, Switzerland.
Laurence FeldmeyerDepartment of Dermatology, Inselspital, Bern University Hospital, University of Bern, 3010 Bern, Switzerland.
Roman SchwobDermFocus, Vetsuisse Faculty, University of Bern, 3008 Bern, Switzerland.
Andrew M OvermillerDepartment of Dermatology and Cutaneous Biology, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Beyza S SayarDepartment of Dermatology, Inselspital, Bern University Hospital, University of Bern, 3010 Bern, Switzerland.
Luca BorradoriDepartment of Dermatology, Inselspital, Bern University Hospital, University of Bern, 3010 Bern, Switzerland.
Mỹ G MahoneyDepartment of Dermatology and Cutaneous Biology, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Arnaud GalichetDepartment of Dermatology, Inselspital, Bern University Hospital, University of Bern, 3010 Bern, Switzerland.
Eliane J MüllerDepartment of Dermatology, Inselspital, Bern University Hospital, University of Bern, 3010 Bern, Switzerland.
University of Bern · CHThomas Jefferson University · USUniversity Hospital of Bern · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stem cells (SCs) are critical to maintain tissue homeostasis. However, it is currently not known whether signaling through cell junctions protects quiescent epithelial SC reservoirs from depletion during disease-inflicted damage. Using the autoimmune model disease pemphigus vulgaris (PV), this study reveals an unprecedented role for a desmosomal cadherin in governing SC quiescence and regeneration through adhesion signaling in the multipotent mouse hair follicle compartment known as the bulge. Autoantibody-mediated, mechanical uncoupling of desmoglein (Dsg) 3 transadhesion activates quiescent bulge SC which lose their multipotency and stemness, become actively cycling, and finally delaminate from their epithelial niche. This then initiates a self-organized regenerative program which restores Dsg3 function and bulge morphology including SC quiescence and multipotency. These profound changes are triggered by the sole loss of functional Dsg3, resemble major signaling events in

Indexed as

Cell biologyMolecular biology

Identifiers

PMID38162019
PMCPMC10755723
OpenAlexW4389000696

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.