Evidence map›Paper›PMID 33766930›Full record

ArticleDevelopment (Cambridge, England)2021

Arid1a regulates cell cycle exit of transit-amplifying cells by inhibiting the Aurka-Cdk1 axis in mouse incisor.

Jiahui Du, Junjun Jing, Shuo Chen, Yuan Yuan, Jifan Feng, Thach-Vu Ho, Prerna Sehgal, Jian Xu, Xinquan Jiang, Yang Chai

Open access · bronzeAbstract read
In one paragraph

Article in Development (Cambridge, England), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. ARID1A and Its Impact Across the Hallmarks of Cancer.International journal of molecular sciences · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Transit Amplifying Cells (TACs): a still not fully understood cell population.Frontiers in bioengineering and biotechnology · 2023
    Review
  11. 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

10 authors at 2 institutions in 2 countries.

Jiahui DuCenter for Craniofacial Molecular Biology, University of Southern California, Los Angeles, CA, 90033, USA.
Junjun JingCenter for Craniofacial Molecular Biology, University of Southern California, Los Angeles, CA, 90033, USA.
Shuo ChenCenter for Craniofacial Molecular Biology, University of Southern California, Los Angeles, CA, 90033, USA.
Yuan YuanCenter for Craniofacial Molecular Biology, University of Southern California, Los Angeles, CA, 90033, USA.
Jifan FengCenter for Craniofacial Molecular Biology, University of Southern California, Los Angeles, CA, 90033, USA.
Thach-Vu HoCenter for Craniofacial Molecular Biology, University of Southern California, Los Angeles, CA, 90033, USA.
Prerna SehgalCenter for Craniofacial Molecular Biology, University of Southern California, Los Angeles, CA, 90033, USA.
Jian XuCenter for Craniofacial Molecular Biology, University of Southern California, Los Angeles, CA, 90033, USA.
Xinquan JiangDepartment of Prosthodontics, Shanghai Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, China.
Yang ChaiCenter for Craniofacial Molecular Biology, University of Southern California, Los Angeles, CA, 90033, USA.
University of Southern California · USShanghai Jiao Tong University · CN

Funding

USC FaceBase III Craniofacial Development and Dysmorpholoy Data Management and Integration HubU01DE028729 · NIDCR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CHAI, YANG, KESSELMAN, CARL · 2019 to 2023
$13.9M
THE MOLECULAR REGULATORY MECHANISM OF TOOTH ROOT DEVELOPMENTR01DE022503 · NIDCR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI Yang Chai · 2012 to 2026
$6.2M
DOCTORAL AND POST-DOCTORAL TRAINING IN CRANIOFACIAL BIOLOGYT90DE021982 · NIDCR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI PAINE, MICHAEL LANSDELL · 2011 to 2025
$6.2M
TGF BETA SIGNALING AND MANDIBULAR MORPHOGENESISR01DE012711 · NIDCR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CHAI, YANG · 1999 to 2023
$5.7M
MOLECULAR REGULATORY MECHANISM OF MESENCHYMAL STEM CELLS IN ADULT MOUSE INCISORSR01DE025221 · NIDCR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI Yang Chai · 2016 to 2026
$4.3M
Protein methylation pathways that control genetic susceptibility to environmental pollutants in the occurrence of craniofacial defectsR01DE030928 · NIDCR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI XU, JIAN · 2021 to 2025
$2.1M
Modulation of Runx2 activity by arginine methylationR21DE028617 · NIDCR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI XU, JIAN · 2019 to 2020
$454k
NIDCR NIH HHS R01 DE012711NIDCR NIH HHS R01 DE022503NIDCR NIH HHS R01 DE025221NIDCR NIH HHS R01 DE030928NIDCR NIH HHS R21 DE028617NIDCR NIH HHS T90 DE021982NIDCR NIH HHS U01 DE028729
6 · The paper itself

Abstract

Stem cells self-renew or give rise to transit-amplifying cells (TACs) that differentiate into specific functional cell types. The fate determination of stem cells to TACs and their transition to fully differentiated progeny is precisely regulated to maintain tissue homeostasis. Arid1a, a core component of the switch/sucrose nonfermentable complex, performs epigenetic regulation of stage- and tissue-specific genes that is indispensable for stem cell homeostasis and differentiation. However, the functional mechanism of Arid1a in the fate commitment of mesenchymal stem cells (MSCs) and their progeny is not clear. Using the continuously growing adult mouse incisor model, we show that Arid1a maintains tissue homeostasis through limiting proliferation, promoting cell cycle exit and differentiation of TACs by inhibiting the Aurka-Cdk1 axis. Loss of Arid1a overactivates the Aurka-Cdk1 axis, leading to expansion of the mitotic TAC population but compromising their differentiation ability. Furthermore, the defective homeostasis after loss of Arid1a ultimately leads to reduction of the MSC population. These findings reveal the functional significance of Arid1a in regulating the fate of TACs and their interaction with MSCs to maintain tissue homeostasis.

Indexed as

MitosisSignal TransductionAnimalsAurora Kinase ACDC2 Protein KinaseDNA-Binding ProteinsIncisorMesenchymal Stem CellsMiceMice, TransgenicTranscription FactorsArid1a protein, mouseAurka protein, mouseAurora Kinase ACDC2 Protein KinaseCdk1 protein, mouseDNA-Binding ProteinsTranscription FactorsArid1aCell cycleMesenchymal stem cellsMitosisTransit-amplifying cells

Identifiers

PMID33766930
PMCPMC8077510
OpenAlexW3138089954

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.