Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV002514249 | SCV003439209 | pathogenic | Achondrogenesis, type IB; Atelosteogenesis type II; Multiple epiphyseal dysplasia type 4; Diastrophic dysplasia | 2022-06-13 | 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: 8571951, 21077204, 21922596). This suggests that this is a clinically significant region of the protein, and that variants that disrupt it are likely to be disease-causing. ClinVar contains an entry for this variant (Variation ID: 56028). This variant is also known as 731-737delGATGGGC. This premature translational stop signal has been observed in individual(s) with SLC26A2-related conditions (PMID: 11241838). This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Met236Serfs*16) in the SLC26A2 gene. While this is not anticipated to result in nonsense mediated decay, it is expected to disrupt the last 504 amino acid(s) of the SLC26A2 protein. |
Baylor Genetics | RCV003474630 | SCV004201780 | likely pathogenic | Achondrogenesis, type IB | 2023-03-18 | criteria provided, single submitter | clinical testing | |
Juha Muilu Group; Institute for Molecular Medicine Finland |
RCV000049437 | SCV000081870 | probable-pathogenic | Diastrophic dysplasia | no assertion criteria provided | not provided | Converted during submission to Likely pathogenic. |