Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Laboratory of Medical Genetics, |
RCV002465392 | SCV002760059 | likely pathogenic | Intellectual disability, autosomal dominant 24 | 2022-11-29 | criteria provided, single submitter | research | |
Gene |
RCV003235728 | SCV003933529 | uncertain significance | not provided | 2022-12-13 | criteria provided, single submitter | clinical testing | Not observed at significant frequency in large population cohorts (gnomAD); In silico analysis supports that this missense variant has a deleterious effect on protein structure/function; This variant is associated with the following publications: (PMID: 31981491) |
Ambry Genetics | RCV004973430 | SCV005563617 | likely pathogenic | Inborn genetic diseases | 2024-11-06 | criteria provided, single submitter | clinical testing | The c.620G>A (p.C207Y) alteration is located in exon 4 (coding exon 4) of the DEAF1 gene. This alteration results from a G to A substitution at nucleotide position 620, causing the cysteine (C) at amino acid position 207 to be replaced by a tyrosine (Y). for autosomal dominant Vulto-van Silfout-de Vries syndrome; however, its clinical significance for autosomal recessive DEAF1-related neurodevelopmental disorder is uncertain. This variant was not reported in population-based cohorts in the Genome Aggregation Database (gnomAD). This variant was reported in multiple individuals with features consistent with Vulto-van Silfout-de Vries syndrome (Zhou, 2022; Abolhassani, 2024). This amino acid position is highly conserved in available vertebrate species. This alteration is predicted to be deleterious by in silico analysis. Based on the available evidence, this alteration is classified as likely pathogenic. |