Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV002601689 | SCV002949886 | pathogenic | Primary open angle glaucoma; Amyotrophic lateral sclerosis type 12; Glaucoma 1, open angle, E | 2022-03-18 | criteria provided, single submitter | clinical testing | This premature translational stop signal has been observed in individual(s) with autosomal recessive amyotrophic lateral sclerosis (PMID: 31759189). It has also been observed to segregate with disease in related individuals. This variant has been reported in individual(s) with autosomal dominant amyotrophic lateral sclerosis (Invitae); however, the role of the variant in this condition is currently unclear. This sequence change creates a premature translational stop signal (p.Glu399*) in the OPTN gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in OPTN are known to be pathogenic (PMID: 20428114). This variant is not present in population databases (gnomAD no frequency). For these reasons, this variant has been classified as Pathogenic. |
Revvity Omics, |
RCV003130726 | SCV003810688 | likely pathogenic | not provided | 2021-12-31 | criteria provided, single submitter | clinical testing | |
Gene |
RCV003130726 | SCV005080615 | pathogenic | not provided | 2023-08-27 | criteria provided, single submitter | clinical testing | Not observed at significant frequency in large population cohorts (gnomAD); 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; This variant is associated with the following publications: (PMID: 31759189) |