Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Baylor Genetics | RCV003472864 | SCV004201775 | likely pathogenic | Achondrogenesis, type IB | 2023-04-18 | criteria provided, single submitter | clinical testing | |
Invitae | RCV003779115 | SCV004570021 | pathogenic | Achondrogenesis, type IB; Atelosteogenesis type II; Multiple epiphyseal dysplasia type 4; Diastrophic dysplasia | 2023-05-05 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. This variant disrupts a region of the SLC26A2 protein in which other variant(s) (p.Ala715Val) have been determined to be pathogenic (PMID: 21077204). This suggests that this is a clinically significant region of the protein, and that variants that disrupt it are likely to be disease-causing. This variant has not been reported in the literature in individuals affected with SLC26A2-related conditions. This variant is present in population databases (rs140041300, gnomAD 0.004%). This sequence change creates a premature translational stop signal (p.Ser285*) in the SLC26A2 gene. While this is not anticipated to result in nonsense mediated decay, it is expected to disrupt the last 455 amino acid(s) of the SLC26A2 protein. |