Evidence map›Paper›PMID 24681597›Full record

ArticleNature medicine2014

Kindlin-1 controls Wnt and TGF-β availability to regulate cutaneous stem cell proliferation.

Emanuel Rognoni, Moritz Widmaier, Madis Jakobson, Raphael Ruppert, Siegfried Ussar, Despoina Katsougkri, Ralph T Böttcher, Joey E Lai-Cheong, Daniel B Rifkin, John A McGrath and 1 more

Open access · greenAbstract read
In one paragraph

Article in Nature medicine, 2014. 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
8.4field-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

74 citing papers in PubMed, 143 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Kindlin Regulates Mechanosensitive Activation and Adhesion Assembly of Integrin beta6.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
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  11. Genes · 2023
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  14. Review
  15. Article
  16. Article
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  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 3 countries.

Emanuel RognoniDepartment of Molecular Medicine, Max Planck Institute of Biochemistry, Martinsried, Germany.
Moritz WidmaierDepartment of Molecular Medicine, Max Planck Institute of Biochemistry, Martinsried, Germany.
Madis JakobsonDepartment of Molecular Medicine, Max Planck Institute of Biochemistry, Martinsried, Germany.
Raphael RuppertDepartment of Molecular Medicine, Max Planck Institute of Biochemistry, Martinsried, Germany.
Siegfried UssarDepartment of Molecular Medicine, Max Planck Institute of Biochemistry, Martinsried, Germany.
Despoina KatsougkriDepartment of Molecular Medicine, Max Planck Institute of Biochemistry, Martinsried, Germany.
Ralph T BöttcherDepartment of Molecular Medicine, Max Planck Institute of Biochemistry, Martinsried, Germany.
Joey E Lai-Cheong1] Department of Dermatology, King Edward VII Hospital, Windsor, UK. [2] St. John's Institute of Dermatology, King's College London (Guy's Campus), London, UK.
Daniel B RifkinNew York University, Langone School of Medicine, New York, New York, USA.
John A McGrathSt. John's Institute of Dermatology, King's College London (Guy's Campus), London, UK.
Reinhard FässlerDepartment of Molecular Medicine, Max Planck Institute of Biochemistry, Martinsried, Germany.
Max Planck Institute of Biochemistry · DEKing's College London · GBNYU Langone Health · US

Funding

Regulation of TGF-Beta Activity in the Lung by LTBP-4R01CA034282 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI RIFKIN, DANIEL B · 1985 to 2016
$5.8M
European Research Council 322652NCI NIH HHS CA034282NCI NIH HHS R01 CA034282Wellcome Trust
6 · The paper itself

Abstract

Kindlin-1 is an integrin tail binding protein that controls integrin activation. Mutations in the FERMT-1 gene, which encodes for Kindlin-1, lead to Kindler syndrome in man, which is characterized by skin blistering, premature skin aging and skin cancer of unknown etiology. Here we show that loss of Kindlin-1 in mouse keratinocytes recapitulates Kindler syndrome and also produces enlarged and hyperactive stem cell compartments, which lead to hyperthickened epidermis, ectopic hair follicle development and increased skin tumor susceptibility. Mechanistically, Kindlin-1 controls keratinocyte adhesion through β1-class integrins and proliferation and differentiation of cutaneous epithelial stem cells by promoting α(v)β(6) integrin-mediated transforming growth factor-β (TGF-β) activation and inhibiting Wnt-β-catenin signaling through integrin-independent regulation of Wnt ligand expression. Our findings assign Kindlin-1 the previously unknown and essential task of controlling cutaneous epithelial stem cell homeostasis by balancing TGF-β-mediated growth-inhibitory signals and Wnt-β-catenin-mediated growth-promoting signals.

Indexed as

BlisterCell ProliferationEpidermolysis BullosaPeriodontal DiseasesPhotosensitivity DisordersAnimalsAntigens, Neoplasmbeta CateninCarrier ProteinsCell AdhesionDisease Models, AnimalHair FollicleIntegrin beta1IntegrinsKeratinocytesMiceAntigens, Neoplasmbeta CateninCarrier Proteinsintegrin alphavbeta6Integrin beta1Integrinskindlin-1 protein, mouseTransforming Growth Factor betaWnt Proteins

Identifiers

PMID24681597
PMCPMC3982140
OpenAlexW2076368781

What OpenQuestion holds

Textmetadata
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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.