Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Baylor Genetics | RCV003465337 | SCV004191656 | likely pathogenic | GNE myopathy | 2023-03-30 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV003767363 | SCV004608706 | pathogenic | GNE myopathy; Sialuria | 2023-01-14 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. This variant disrupts the p.Ala622 amino acid residue in GNE. Other variant(s) that disrupt this residue have been observed in individuals with GNE-related conditions (PMID: 30390020), which suggests that this may be a clinically significant amino acid residue. Algorithms developed to predict the effect of missense changes on protein structure and function (SIFT, PolyPhen-2, Align-GVGD) all suggest that this variant is likely to be disruptive. ClinVar contains an entry for this variant (Variation ID: 498575). This variant is also known as p.A591T. This missense change has been observed in individual(s) with autosomal recessive GNE-related conditions (PMID: 16372135, 21868336, 30390020, 31286697). In at least one individual the data is consistent with being in trans (on the opposite chromosome) from a pathogenic variant. This variant is present in population databases (rs752286512, gnomAD 0.002%). This sequence change replaces alanine, which is neutral and non-polar, with threonine, which is neutral and polar, at codon 622 of the GNE protein (p.Ala622Thr). |
Juno Genomics, |
RCV003465337 | SCV005418906 | likely pathogenic | GNE myopathy | criteria provided, single submitter | clinical testing | PM2_Supporting+PP3+PM3+PP4+PP1 | |
Eurofins Ntd Llc |
RCV000595256 | SCV000703655 | uncertain significance | not provided | 2016-12-06 | flagged submission | clinical testing |