ArticleJournal of molecular medicine (Berlin, Germany)2024
New CRISPR/Cas9-based Fgfr2
Article in Journal of molecular medicine (Berlin, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Fzd7 Restrains Pink1-Dependent Mitophagy in Suture Stem Cells to Maintain Cranial Suture Patency.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mitochondria-related gene and protein changes in craniosynostosis: integrated transcriptomics and Fgfr2C361Y/+ cranial suture proteomics.Functional & integrative genomics · 2026Article
- Spatiotemporal single-cell atlas of suture stem cell dynamics in craniosynostosis.Stem cell research & therapy · 2026Article
- Unraveling the FGFR-RNA splicing axis: Mechanisms, oncogenic crosstalks and innovations for therapeutic purpose.Acta pharmaceutica Sinica. B · 2026Review
- Human cranial stem cells: developmental, pathologic, and therapeutic implications.Frontiers in cell and developmental biology · 2026Review
- P38α MAPK-induced senescence in cranial suture progenitor cells promotes craniosynostosis.Communications biology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Crouzon syndrome (CS), a syndromic craniosynostosis, is a craniofacial developmental deformity caused by mutations in fibroblast growth factor receptor 2 (FGFR2). Previous CS mouse models constructed using traditional gene editing techniques faced issues such as low targeting efficiency, extended lineage cycles, and inconsistent and unstable phenotypes. In this study, a CRISPR/Cas9-mediated strategy was employed to induce a functional augmentation of the Fgfr2 point mutation in mice. Various techniques, including bone staining, micro-CT, histological methods, and behavioral experiments, were employed to systematically examine and corroborate phenotypic disparities between mutant mice (Fgfr2
Indexed as
Identifiers
39158595What Socratic 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 Socratic graph.