Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Institute of Human Genetics, |
RCV003595849 | SCV004263874 | likely pathogenic | Fetal akinesia, respiratory insufficiency, microcephaly, polymicrogyria, and dysmorphic facies | 2024-02-09 | criteria provided, single submitter | clinical testing | |
Gene |
RCV004593377 | SCV005078276 | likely pathogenic | not provided | 2023-10-19 | criteria provided, single submitter | clinical testing | 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 at significant frequency in large population cohorts (gnomAD); Has not been previously published as pathogenic or benign in association with neurodevelopmental disorders to our knowledge; This variant is associated with the following publications: (PMID: 24463508) |
Labcorp Genetics |
RCV005101422 | SCV005820039 | pathogenic | Familial hemiplegic migraine | 2024-05-15 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg493*) in the ATP1A2 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in ATP1A2 are known to be pathogenic (PMID: 30690204). This variant is present in population databases (rs534696343, gnomAD 0.002%). This variant has not been reported in the literature in individuals affected with ATP1A2-related conditions. For these reasons, this variant has been classified as Pathogenic. |