| Literature DB >> 32435055 |
Nina N Brodsky1,2, Oksana Boyarchuk3, Tetyana Kovalchuk4, Tetyana Hariyan4, Andrew Rice1, Weizhen Ji2,5, Mustafa Khokha2,5, Saquib Lakhani2,5, Carrie L Lucas6,7.
Abstract
Two variants in the ubiquitously expressed NHLRC2 gene have been reported to cause a lethal fibrotic cerebropulmonary disease termed fibrosis, neurodegeneration, and cerebral angiomatosis (FINCA) syndrome in three Finnish children. Our objective was to determine the genetic basis of disease in a new patient with clinical features of FINCA syndrome using whole-exome sequencing (WES) and confirmation by Sanger sequencing. The patient has one known and one novel variant in NHLRC2 (c.442T>G, p.D148Y and c.428C>A, p.H143P, respectively). p.H143P is extremely rare and is not present in the gnomAD database of >140,000 allele sequences from healthy humans. Both variants affect the highly conserved N-terminal thioredoxin (Trx)-like domain of NHLRC2 and are predicted to be damaging. We conclude that a compound heterozygous combination of a known and a novel variant in NHLRC2 causes FINCA syndrome in a 2-year-old Ukrainian patient, underscoring the importance of NHLRC2 as a central regulator of fibrosis.Entities:
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Year: 2020 PMID: 32435055 DOI: 10.1038/s10038-020-0776-0
Source DB: PubMed Journal: J Hum Genet ISSN: 1434-5161 Impact factor: 3.172