ArticleEuropean journal of human genetics : EJHG2024
The phenotype of MEGF8-related Carpenter syndrome (CRPT2) is refined through the identification of eight new patients.
Article in European journal of human genetics : EJHG, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Beyond the Negative: Insights From Postnatal Medical Genetics Follow-Up After Nondiagnostic Prenatal Exome Sequencing.Prenatal diagnosis · 2026Article
- MEGF8 controls osteogenic differentiation through post-transcriptional regulation of BMP-SMAD signaling in craniosynostosis.Cell death and differentiation · 2026Article
- Design principles of a membrane-spanning ubiquitin ligase.Molecular cell · 2026Article
- Structural and functional brain asymmetry in relation to heterogeneous causes of situs inversus totalis.Brain structure & function · 2026Article
- "Design principles of a membrane-spanning ubiquitin ligase".bioRxiv : the preprint server for biology · 2025Article
- Hitting the heights with CiteScore.European journal of human genetics : EJHG · 2024Article
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Authors and funding
14 authors.
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Abstract
Carpenter syndrome (CRPTS) is a rare autosomal recessive condition caused by biallelic variants in genes that encode negative regulators of hedgehog signalling (RAB23 [CRPT1] or, more rarely, MEGF8 [CRPT2]), and is characterised by craniosynostosis, polysyndactyly, and other congenital abnormalities. We describe a further six families comprising eight individuals with MEGF8-associated CRPT2, increasing the total number of reported cases to fifteen, and refine the phenotype of CRPT2 compared to CRPT1. The core features of craniosynostosis, polysyndactyly and (in males) cryptorchidism are almost universal in both CRPT1 and CRPT2. However, laterality defects are present in nearly half of those with MEGF8-associated CRPT2, but are rare in RAB23-associated CRPT1. Craniosynostosis in CRPT2 commonly involves a single midline suture in comparison to the multi-suture craniosynostosis characteristic of CRPT1. No patient to date has carried two MEGF8 gene alterations that are both predicted to lead to complete loss-of-function, suggesting that a variable degree of residual MEGF8 activity may be essential for viability and potentially contributing to variable phenotypic severity. These data refine the phenotypic spectrum of CRPT2 in comparison to CRPT1 and more than double the number of likely pathogenic MEGF8 variants in this rare disorder.
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