Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
3billion, |
RCV002251195 | SCV002521698 | pathogenic | Achromatopsia 2 | 2022-05-22 | criteria provided, single submitter | clinical testing | The variant is observed at an extremely low frequency in the gnomAD v2.1.1 dataset (total allele frequency: 0.002%). Stop-gained (nonsense): predicted to result in a loss or disruption of normal protein function through nonsense-mediated decay (NMD) or protein truncation. Multiple pathogenic variants are reported downstream of the variant. The variant has been reported to be associated with CNGA3 related disorder (PMID: 24903488). Therefore, this variant is classified as pathogenic according to the recommendation of ACMG/AMP guideline. |
Labcorp Genetics |
RCV003101371 | SCV003524936 | pathogenic | not provided | 2024-07-04 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Ser21*) in the CNGA3 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in CNGA3 are known to be pathogenic (PMID: 14757870, 24903488, 25637600). This variant is present in population databases (no rsID available, gnomAD 0.03%). This premature translational stop signal has been observed in individual(s) with CNGA3-related conditions (PMID: 24903488, 25637600). This variant is also known as p.S31X. ClinVar contains an entry for this variant (Variation ID: 1687513). For these reasons, this variant has been classified as Pathogenic. |