ArticleClinical genetics2026
RNA Analysis Uncovers Pathogenic PARN Variant in Dyskeratosis Congenita.
Article in Clinical genetics, 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.
- RNA Analysis Uncovers Pathogenic PARN Variant in Dyskeratosis Congenita.Clinical genetics · 2026Article
- Hematological complications in solid organ transplant recipients with telomere biology disorders: a narrative review.Frontiers in immunology · 2025Review
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
Dyskeratosis congenita (DC) is a rare genetic disorder caused by impaired telomere maintenance, leading to diverse clinical manifestations, including bone marrow failure, mucocutaneous abnormalities, and multi-organ dysfunction. Here, we report a 14-year-old male patient presenting with microcephaly, developmental delay, synostoses, cerebellar hypoplasia with ataxia, and an immunodeficiency condition, but lacking classical DC features such as nail dystrophy and skin hyperpigmentation. WGS revealed two variants in the PARN gene: a known pathogenic missense variant (c.1045C > T, p.Arg349Trp) and a novel intronic variant (c.178-28T > C). Functional RNA analysis demonstrated that the intronic variant disrupts the branch point sequence, leading to exon 4 skipping and nonsense-mediated decay (NMD) of a significant proportion of transcripts. This study confirms the pathogenicity of the intronic variant and underscores the importance of functional validation in interpreting noncoding variants, particularly in genetically heterogeneous disorders like DC. Our findings expand the molecular and phenotypic spectrum of PARN-related DC and highlight the utility of WGS reanalysis and RNA studies in resolving diagnostically challenging cases.
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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.