Evidence map›Paper›PMID 29496737›Full record

ArticleThe Journal of cell biology2018

Kindlin-2 regulates mesenchymal stem cell differentiation through control of YAP1/TAZ.

Ling Guo, Ting Cai, Keng Chen, Rong Wang, Jiaxin Wang, Chunhong Cui, Jifan Yuan, Kuo Zhang, Zhongzhen Liu, Yi Deng and 2 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

60 citing papers in PubMed, 86 citations in OpenAlex.

  1. Article
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  4. Review
  5. Article
  6. Article
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  8. Article
  9. M2c Macrophages Mediate YAP1 to Promote Vascularized Bone Regeneration in Distraction Osteogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
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  12. Article
  13. Review
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  15. Article
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  18. Article
  19. Review
  20. Osteoarthritis: pathogenic signaling pathways and therapeutic targets.Signal transduction and targeted therapy · 2023
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 3 institutions in 2 countries.

Ling GuoGuangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, and Department of Biology, Southern University of Science and Technology, Shenzhen, China.
Ting CaiGuangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, and Department of Biology, Southern University of Science and Technology, Shenzhen, China.
Keng ChenGuangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, and Department of Biology, Southern University of Science and Technology, Shenzhen, China.
Rong WangGuangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, and Department of Biology, Southern University of Science and Technology, Shenzhen, China.
Jiaxin WangGuangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, and Department of Biology, Southern University of Science and Technology, Shenzhen, China.ORCID 0000-0001-6217-635X
Chunhong CuiGuangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, and Department of Biology, Southern University of Science and Technology, Shenzhen, China.
Jifan YuanGuangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, and Department of Biology, Southern University of Science and Technology, Shenzhen, China.
Kuo ZhangGuangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, and Department of Biology, Southern University of Science and Technology, Shenzhen, China.
Zhongzhen LiuGuangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, and Department of Biology, Southern University of Science and Technology, Shenzhen, China.
Yi DengGuangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, and Department of Biology, Southern University of Science and Technology, Shenzhen, China.
Guozhi XiaoGuangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, and Department of Biology, Southern University of Science and Technology, Shenzhen, China.ORCID 0000-0001-8903-0609
Chuanyue WuGuangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, and Department of Biology, Southern University of Science and Technology, Shenzhen, China wucy@sustc.edu.cn.ORCID 0000-0003-2536-4014
Southern University of Science and Technology · CNRush University Medical Center · USUniversity of Pittsburgh · US

Funding

Signaling Mechanisms of Focal Adhesion Protein Kindlin-2 in ChondrogenesisR01AR068950 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HUANG, JIAN, WU, CHUANYUE · 2015 to 2019
$2.2M
NIAMS NIH HHS R01 AR068950
6 · The paper itself

Abstract

Precise control of mesenchymal stem cell (MSC) differentiation is critical for tissue development and regeneration. We show here that kindlin-2 is a key determinant of MSC fate decision. Depletion of kindlin-2 in MSCs is sufficient to induce adipogenesis and inhibit osteogenesis in vitro and in vivo. Mechanistically, kindlin-2 regulates MSC differentiation through controlling YAP1/TAZ at both the transcript and protein levels. Kindlin-2 physically associates with myosin light-chain kinase in response to mechanical cues of cell microenvironment and intracellular signaling events and promotes myosin light-chain phosphorylation. Loss of kindlin-2 inhibits RhoA activation and reduces myosin light-chain phosphorylation, stress fiber formation, and focal adhesion assembly, resulting in increased Ser127 phosphorylation, nuclear exclusion, and ubiquitin ligase atrophin-1 interacting protein 4-mediated degradation of YAP1/TAZ. Our findings reveal a novel kindlin-2 signaling axis that senses the mechanical cues of cell microenvironment and controls MSC fate decision, and they suggest a new strategy to regulate MSC differentiation, tissue repair, and regeneration.

Indexed as

Cell DifferentiationCell LineageAdaptor Proteins, Signal TransducingAdipogenesisAnimalsCell Cycle ProteinsCytoskeletal ProteinsFocal AdhesionsHEK293 CellsHomeodomain ProteinsHumansIntracellular Signaling Peptides and ProteinsMechanotransduction, CellularMembrane ProteinsMesenchymal Stem CellsMice, KnockoutAdaptor Proteins, Signal TransducingCell Cycle ProteinsCytoskeletal ProteinsFERMT3 protein, humanHomeodomain ProteinsIntracellular Signaling Peptides and ProteinsITCH protein, humankindlin-2 protein, mouseMembrane ProteinsMuscle ProteinsMyosin-Light-Chain KinaseMyosin Light ChainsNeoplasm ProteinsPhosphoproteinsPrrx1 protein, mouseRepressor ProteinsrhoA GTP-Binding ProteinRHOA protein, humanTrans-ActivatorsTranscriptional Coactivator with PDZ-Binding Motif ProteinsTranscription FactorsUbiquitin-Protein LigasesWWTR1 protein, humanWwtr1 protein, mouseYAP1 protein, humanYap1 protein, mouseYAP-Signaling Proteins

Identifiers

PMID29496737
PMCPMC5881491
OpenAlexW2790905309

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.