Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Ce |
RCV001090802 | SCV001246532 | pathogenic | not provided | 2016-12-01 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001256643 | SCV002238203 | pathogenic | Leber congenital amaurosis 9 | 2023-03-08 | 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: 871050). This variant is also known as c.362delA (p.Glu121Glufs*20). This premature translational stop signal has been observed in individual(s) with Leber congenital amaurosis (PMID: 22842229, 29178642). In at least one individual the data is consistent with being in trans (on the opposite chromosome) from a pathogenic variant. This variant is present in population databases (no rsID available, gnomAD 0.002%). This sequence change creates a premature translational stop signal (p.Arg122Glyfs*20) in the NMNAT1 gene. While this is not anticipated to result in nonsense mediated decay, it is expected to disrupt the last 158 amino acid(s) of the NMNAT1 protein. |
Laboratory of Genetics in Ophthalmology, |
RCV001256643 | SCV001433015 | pathogenic | Leber congenital amaurosis 9 | no assertion criteria provided | research | ||
Genomics England Pilot Project, |
RCV001256643 | SCV001759972 | pathogenic | Leber congenital amaurosis 9 | no assertion criteria provided | clinical testing |