Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Eurofins Ntd Llc |
RCV000324846 | SCV000332972 | pathogenic | not provided | 2015-07-16 | criteria provided, single submitter | clinical testing | |
Revvity Omics, |
RCV001782773 | SCV002025244 | likely pathogenic | UDPglucose-4-epimerase deficiency | 2021-02-24 | criteria provided, single submitter | clinical testing | |
Fulgent Genetics, |
RCV001782773 | SCV002780656 | likely pathogenic | UDPglucose-4-epimerase deficiency | 2022-03-15 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001782773 | SCV004676655 | likely pathogenic | UDPglucose-4-epimerase deficiency | 2023-09-08 | criteria provided, single submitter | clinical testing | This variant is present in population databases (rs779828095, gnomAD 0.002%). This sequence change affects an acceptor splice site in intron 9 of the GALE gene. It is expected to disrupt RNA splicing. Variants that disrupt the donor or acceptor splice site typically lead to a loss of protein function (PMID: 16199547), and loss-of-function variants in GALE are known to be pathogenic (PMID: 16301867). This variant has not been reported in the literature in individuals affected with GALE-related conditions. ClinVar contains an entry for this variant (Variation ID: 281922). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus splice site. In summary, the currently available evidence indicates that the variant is pathogenic, but additional data are needed to prove that conclusively. Therefore, this variant has been classified as Likely Pathogenic. |