Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001906059 | SCV002162519 | pathogenic | not provided | 2023-11-10 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.His916Glnfs*7) in the SLC12A3 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in SLC12A3 are known to be pathogenic (PMID: 20848653, 22009145, 25841442). This variant is present in population databases (rs750735794, gnomAD 0.005%). This premature translational stop signal has been observed in individual(s) with Gitelman syndrome (PMID: 10988270). ClinVar contains an entry for this variant (Variation ID: 1397263). For these reasons, this variant has been classified as Pathogenic. |
Fulgent Genetics, |
RCV002506984 | SCV002814460 | pathogenic | Familial hypokalemia-hypomagnesemia | 2021-12-16 | criteria provided, single submitter | clinical testing | |
Gene |
RCV001906059 | SCV004035421 | pathogenic | not provided | 2023-08-04 | criteria provided, single submitter | clinical testing | Frameshift variant predicted to result in protein truncation or nonsense mediated decay in a gene for which loss of function is a known mechanism of disease; This variant is associated with the following publications: (PMID: 10988270) |
Clinical Genetics Laboratory, |
RCV001906059 | SCV005197552 | pathogenic | not provided | 2022-07-13 | criteria provided, single submitter | clinical testing |