Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Molecular Medicine for Neurodegenerative and Neuromuscular Diseases Unit, |
RCV001647226 | SCV001519124 | pathogenic | Autosomal recessive ataxia due to ubiquinone deficiency | 2021-01-04 | criteria provided, single submitter | research | |
Labcorp Genetics |
RCV002546249 | SCV003524121 | pathogenic | not provided | 2022-10-17 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. Variants that disrupt the consensus splice site are a relatively common cause of aberrant splicing (PMID: 17576681, 9536098). Studies have shown that this variant is associated with altered splicing resulting in unknown protein product impact (PMID: 24164873). ClinVar contains an entry for this variant (Variation ID: 1027504). This variant has been observed in individuals with clinical features of primary coenzyme Q10 deficiency (PMID: 24164873, 31890231, 32337771). This variant is present in population databases (no rsID available, gnomAD 0.007%). This sequence change falls in intron 3 of the COQ8A gene. It does not directly change the encoded amino acid sequence of the COQ8A protein. It affects a nucleotide within the consensus splice site. |