Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000401792 | SCV000330224 | pathogenic | not provided | 2022-08-19 | criteria provided, single submitter | clinical testing | Identified in an infant with CoQ10 deficiency who harbored a likely pathogenic variant on the opposite allele (in trans) (Sondheimer et al., 2017); Frameshift 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: 28540186) |
Labcorp Genetics |
RCV001855066 | SCV002244751 | pathogenic | Neonatal encephalomyopathy-cardiomyopathy-respiratory distress syndrome | 2023-08-17 | 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: 280320). This premature translational stop signal has been observed in individual(s) with coenzyme Q10 deficiency (PMID: 28540186). This variant is present in population databases (no rsID available, gnomAD 0.004%). This sequence change creates a premature translational stop signal (p.Val8Alafs*19) in the COQ4 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in COQ4 are known to be pathogenic (PMID: 25658047). |
Fulgent Genetics, |
RCV005049510 | SCV005679925 | pathogenic | Neonatal encephalomyopathy-cardiomyopathy-respiratory distress syndrome; Spastic ataxia 10, autosomal recessive | 2024-01-25 | criteria provided, single submitter | clinical testing |