Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001371665 | SCV001568237 | pathogenic | not provided | 2022-08-31 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. ClinVar contains an entry for this variant (Variation ID: 1061997). This premature translational stop signal has been observed in individual(s) with autosomal dominant optic atrophy (PMID: 34056600). This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Arg378*) in the ACO2 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in ACO2 are known to be pathogenic (PMID: 30689204, 32519519). |
Gene |
RCV001371665 | SCV002031040 | pathogenic | not provided | 2023-07-03 | criteria provided, single submitter | clinical testing | Identified in the heterozygous state in a patient with optic neuropathy in the literature; the variant was also noted to be heterozygous in an asymptomatic parent (Charif et al., 2021); Nonsense 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 in large population cohorts (gnomAD); This variant is associated with the following publications: (PMID: 27535533, 34056600) |
Revvity Omics, |
RCV001371665 | SCV003822503 | uncertain significance | not provided | 2022-01-10 | criteria provided, single submitter | clinical testing |