Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV001558587 | SCV001780570 | pathogenic | not provided | 2023-06-22 | 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); This variant is associated with the following publications: (PMID: 22310368, 16213125, 25525159, 22272371, 22523683, 20382551, 19703648, 19255735, 11349233, 36403546, 35551180, 34670123) |
Institute of Human Genetics, |
RCV000043635 | SCV002102457 | pathogenic | Mitochondrial complex 1 deficiency, nuclear type 5 | 2022-02-22 | criteria provided, single submitter | clinical testing | This variant was identified as compound heterozygous with NM_005006.7:c.2006A>G._x000D_ Criteria applied: PVS1, PM3, PM2_SUP |
Labcorp Genetics |
RCV001558587 | SCV003292302 | pathogenic | not provided | 2022-09-03 | criteria provided, single submitter | clinical testing | ClinVar contains an entry for this variant (Variation ID: 50923). For these reasons, this variant has been classified as Pathogenic. This premature translational stop signal has been observed in individual(s) with mitochondrial complex I deficiency (PMID: 11349233). This variant is present in population databases (rs372691318, gnomAD 0.003%). This sequence change creates a premature translational stop signal (p.Arg557*) in the NDUFS1 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in NDUFS1 are known to be pathogenic (PMID: 11349233, 22200994). |
OMIM | RCV000043635 | SCV000071660 | pathogenic | Mitochondrial complex 1 deficiency, nuclear type 5 | 2010-07-01 | no assertion criteria provided | literature only |