Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001035507 | SCV001198836 | pathogenic | not provided | 2019-11-28 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. Loss-of-function variants in SLC12A3 are known to be pathogenic (PMID: 20848653, 22009145, 25841442). This variant has not been reported in the literature in individuals with SLC12A3-related conditions. This variant is not present in population databases (ExAC no frequency). This sequence change creates a premature translational stop signal (p.Tyr438*) in the SLC12A3 gene. It is expected to result in an absent or disrupted protein product. |
Sydney Genome Diagnostics, |
RCV001328171 | SCV001449430 | pathogenic | Familial hypokalemia-hypomagnesemia; Bartter syndrome | 2018-05-03 | no assertion criteria provided | clinical testing | This patient is heterozygous for the c.1314C>G variant in the SLC12A3 gene. This variant creates a premature stop codon (p.Tyr438*) and may result in a null allele due to nonsense-mediated mRNA decay. To our knowledge, this variant has not been previously reported to be a disease causing variant and it has not been reported in the ExAC allele frequency database (http://exac.broadinstitute.org). According to ACMG guidelines, this variant is considered to be pathogenic. |