Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Fulgent Genetics, |
RCV002493399 | SCV002808700 | pathogenic | Mitochondrial complex 1 deficiency, nuclear type 5 | 2022-02-27 | criteria provided, single submitter | clinical testing | |
Juno Genomics, |
RCV002493399 | SCV005440568 | pathogenic | Mitochondrial complex 1 deficiency, nuclear type 5 | criteria provided, single submitter | clinical testing | PM2_Supporting+PVS1+PM3_Supporting+PP4 | |
Labcorp Genetics |
RCV005092207 | SCV005734130 | pathogenic | not provided | 2024-09-20 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg22*) 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). This variant is present in population databases (rs750971390, gnomAD 0.03%). This premature translational stop signal has been observed in individual(s) with clinical features of NDUFS1-related conditions (PMID: 31178897). ClinVar contains an entry for this variant (Variation ID: 626277). For these reasons, this variant has been classified as Pathogenic. |
Biochemistry Laboratory of CDMU, |
RCV000768438 | SCV000899196 | pathogenic | Mitochondrial complex I deficiency, nuclear type 1 | no assertion criteria provided | case-control |