Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001384058 | SCV001583431 | pathogenic | Senior-Loken syndrome 7; Bardet-Biedl syndrome 16 | 2022-08-22 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may create or strengthen a splice site. ClinVar contains an entry for this variant (Variation ID: 1071556). This variant has not been reported in the literature in individuals affected with SDCCAG8-related conditions. This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Gln383*) in the SDCCAG8 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in SDCCAG8 are known to be pathogenic (PMID: 20835237, 22190896). |
Fulgent Genetics, |
RCV001384058 | SCV002813312 | likely pathogenic | Senior-Loken syndrome 7; Bardet-Biedl syndrome 16 | 2022-03-14 | criteria provided, single submitter | clinical testing | |
Prevention |
RCV004734163 | SCV005341706 | likely pathogenic | SDCCAG8-related disorder | 2024-02-27 | no assertion criteria provided | clinical testing | The SDCCAG8 c.1147C>T variant is predicted to result in premature protein termination (p.Gln383*). This variant has not been reported in a large population database, indicating this variant is rare. Nonsense variants in SDCCAG8 are expected to be pathogenic. This variant is interpreted as likely pathogenic. |