Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV002274547 | SCV002559331 | pathogenic | not provided | 2022-08-04 | 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; Not observed at significant frequency in large population cohorts (gnomAD); This variant is associated with the following publications: (PMID: 20694819, 12414817, 26846157, 29440549, 19639346, 34159584, 28233610) |
Labcorp Genetics |
RCV002274547 | SCV003299460 | pathogenic | not provided | 2022-10-21 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Tyr396Thrfs*12) in the ATP6V0A4 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in ATP6V0A4 are known to be pathogenic (PMID: 12414817, 16611712). This variant is present in population databases (rs566440675, gnomAD 0.003%). This premature translational stop signal has been observed in individual(s) with renal tubular acidosis (PMID: 34159584). ClinVar contains an entry for this variant (Variation ID: 1700298). For these reasons, this variant has been classified as Pathogenic. |