ReviewGenesis (New York, N.Y. : 2000)2013
Determining how defects in connexin43 cause skeletal disease.
Review in Genesis (New York, N.Y. : 2000), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 14 citations in OpenAlex.
- Ccn2a acts downstream of cx43 to influence joint formation during zebrafish fin regeneration.Biology open · 2025Article
- Review
- Simplet-dependent regulation of β-catenin signaling influences skeletal patterning downstream of Cx43.Development (Cambridge, England) · 2018Article
- Cohesin mediates Esco2-dependent transcriptional regulation in a zebrafish regenerating fin model of Roberts Syndrome.Biology open · 2017Article
- Cx43 suppresses evx1 expression to regulate joint initiation in the regenerating fin.Developmental dynamics : an official publication of the American Association of Anatomists · 2017Article
- Role of connexins and pannexins during ontogeny, regeneration, and pathologies of bone.BMC cell biology · 2016Review
- Connexins and pannexins in the skeleton: gap junctions, hemichannels and more.Cellular and molecular life sciences : CMLS · 2015Review
- The art of fin regeneration in zebrafish.Regeneration (Oxford, England) · 2015Review
- Gap junctional regulation of signal transduction in bone cells.FEBS letters · 2014Review
- Molecular mechanisms of osteoblast/osteocyte regulation by connexin43.Calcified tissue international · 2014Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Gap junction channels mediate direct cell-cell communication via the exchange of second messengers, ions, and metabolites from one cell to another. Mutations in several human connexin (cx) genes, the subunits of gap junction channels, disturb the development and function of multiple tissues/organs. In particular, appropriate function of Cx43 is required for skeletal development in all vertebrate model organisms. Importantly, it remains largely unclear how disruption of gap junctional intercellular communication causes developmental defects. Two groups have taken distinct approaches toward defining the tangible molecular changes occurring downstream of Cx43-based gap junctional communication. Here, these strategies for determining how Cx43 modulates downstream events relevant to skeletal morphogenesis were reviewed.
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.