ArticleCell reports2021
Arid1a-Plagl1-Hh signaling is indispensable for differentiation-associated cell cycle arrest of tooth root progenitors.
Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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.
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.
Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- The PLAGL1-KLF4-IRX5 axis promotes the osteogenesis of periosteal progenitors during mandible regeneration.Nature communications · 2026Article
- Depletion of macrophages during early postnatal development leads to disrupted tooth root development and altered Gli1⁺ MSC trajectory.Cell death & disease · 2026Article
- Article
- PLAGL1-IGF2 axis regulates osteogenesis of postnatal condyle development.International journal of oral science · 2025Article
- Article
- Enhancer-driven Shh signaling promotes glia-to-mesenchyme transition during bone repair.Bone research · 2025Article
- Identification of a DNA methylation signature in whole blood of newborn guinea pigs and human neonates following antenatal betamethasone exposure.Translational psychiatry · 2024Article
- ARID1A safeguards the canalization of the cell fate decision during osteoclastogenesis.Nature communications · 2024Article
- Spatiotemporal cellular dynamics and molecular regulation of tooth root ontogeny.International journal of oral science · 2023Review
- An Unusual Gingival (Peripheral) Tumor with Features of Keratoameloblastoma with Cytologic Atypia or Possible Malignant Transformation Exhibiting ARID1A Mutation.Head and neck pathology · 2023Article
- The Role of Genetic Mutations in Mitochondrial-Driven Cancer Growth in Selected Tumors: Breast and Gynecological Malignancies.Life (Basel, Switzerland) · 2023Review
- BRD9-mediated chromatin remodeling suppresses osteoclastogenesis through negative feedback mechanism.Nature communications · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Chromatin remodelers often show broad expression patterns in multiple cell types yet can elicit cell-specific effects in development and diseases. Arid1a binds DNA and regulates gene expression during tissue development and homeostasis. However, it is unclear how Arid1a achieves its functional specificity in regulating progenitor cells. Using the tooth root as a model, we show that loss of Arid1a impairs the differentiation-associated cell cycle arrest of tooth root progenitors through Hedgehog (Hh) signaling regulation, leading to shortened roots. Our data suggest that Plagl1, as a co-factor, endows Arid1a with its cell-type/spatial functional specificity. Furthermore, we show that loss of Arid1a leads to increased expression of Arid1b, which is also indispensable for odontoblast differentiation but is not involved in regulation of Hh signaling. This study expands our knowledge of the intricate interactions among chromatin remodelers, transcription factors, and signaling molecules during progenitor cell fate determination and lineage commitment.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.