ArticleCalcified tissue international2026
Impaired Remodeling of Tight Junctions Associated with Loss of Enamel Rod Decussation in Tgfbr2
Article in Calcified tissue international, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
2 citing papers in PubMed.
- Preclinical modeling of Loeys-Dietz syndrome: insights into mechanisms and therapy.Orphanet journal of rare diseases · 2026Review
- Editorial "Enamel" Issue.Calcified tissue international · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
During enamel secretion, ameloblasts follow a complex coordinated movement that results in the enamel rods being arranged in a crisscross pattern that contributes significantly to its exceptional mechanical properties. We previously determined that mutations in the gene encoding TGF-β receptor 2 (TGFR-2) in humans (TGFBR2) and mice (Tgfbr2) result in the formation of fully mineralized enamel that exhibits impaired decussation of enamel rods. Using Tgfbr2
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Registered trials
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