Evidence map›Paper›PMID 24338011›Full record

ArticleThe Journal of biological chemistry2014

Pannexin 3 inhibits proliferation of osteoprogenitor cells by regulating Wnt and p21 signaling.

Masaki Ishikawa, Tsutomu Iwamoto, Satoshi Fukumoto, Yoshihiko Yamada

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

30 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Pannexin channels in inflammation and tumorigenesis.Frontiers in cell and developmental biology · 2025
    Review
  3. Review
  4. Article
  5. Article
  6. Pannexin 3 channels in health and disease.Purinergic signalling · 2021
    Review
  7. ATP transporters in the joints.Purinergic signalling · 2021
    Review
  8. Review
  9. Article
  10. Pannexin 1 Influences Lineage Specification of Human iPSCs.Frontiers in cell and developmental biology · 2021
    Article
  11. Pannexin 3 ER CaScientific reports · 2019
    Article
  12. Gap Junctions and Wnt Signaling in the Mammary Gland: a Cross-Talk?Journal of mammary gland biology and neoplasia · 2019
    Review
  13. Review
  14. Article
  15. Analysis of CaJournal of bone and mineral metabolism · 2018
    Article
  16. Review
  17. Human stem cells express pannexins.BMC research notes · 2018
    Article
  18. The Role of Pannexin 3 in Bone Biology.Journal of dental research · 2017
    Review
  19. Article
  20. 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

4 authors at 3 institutions in 2 countries.

Masaki IshikawaFrom the Laboratory of Cell and Developmental Biology, NIDCR, National Institutes of Health, Bethesda, Maryland 20892-4370.
Tsutomu Iwamoto
Satoshi Fukumoto
Yoshihiko Yamada
National Institutes of Health · USTohoku University · JPTokushima University · JP

Funding

Cartilage Development and DiseaseZIADE000483 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI YAMADA, YOSHIHIKO · 2009 to 2017
$5.9M
Intramural NIH HHS
6 · The paper itself

Abstract

Canonical Wnt signaling and BMP promote the proliferation and differentiation of osteoprogenitors, respectively. However, the regulatory mechanism involved in the transition from proliferation to differentiation is unclear. Here, we show that Panx3 (pannexin 3) plays a key role in this transition by inhibiting the proliferation and promoting the cell cycle exit. Using primary calvarial cells and explants, C3H10T1/2 cells, and C2C12 cells, we found that Panx3 expression inhibited cell growth, whereas the inhibition of endogenous Panx3 expression increased it. We also found that the Panx3 hemichannel inhibited cell growth by promoting β-catenin degradation through GSK3β activation. Additionally, the Panx3 hemichannel inhibited cyclin D1 transcription and Rb phosphorylation through reduced cAMP/PKA/CREB signaling. Furthermore, the Panx3 endoplasmic reticulum Ca(2+) channel induced the transcription and phosphorylation of p21, through the calmodulin/Smad pathway, and resulted in the cell cycle exit. Our results reveal that Panx3 is a new regulator that promotes the switch from proliferation to differentiation of osteoprogenitors via multiple Panx3 signaling pathways.

Indexed as

AnimalsAnimals, Newbornbeta CateninCalciumCell Cycle CheckpointsCell DifferentiationCell LineCell ProliferationConnexinsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaMiceMice, Inbred C3HMice, Inbred C57BLOrgan Culture TechniquesOsteocytesbeta CateninCalciumConnexinsCTNNB1 protein, mouseGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, mousep21-Activated Kinasespannexin 3 protein, mouseATPCalcium Intracellular ReleaseCell ProliferationHemichannel and ER Ca2+ ChannelIntracellular ATP and Ca2+ levelsp21PannexinPannexin 3Wnt SignalingWnt/β-Catenin Signaling

Identifiers

PMID24338011
PMCPMC3908416
OpenAlexW2047960556

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.