Total submissions: 8
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Institute of Human Genetics Munich, |
RCV000995747 | SCV001150075 | pathogenic | Mitochondrial complex IV deficiency, nuclear type 1 | 2018-08-20 | criteria provided, single submitter | clinical testing | |
Kids Research, |
RCV000995747 | SCV001244720 | pathogenic | Mitochondrial complex IV deficiency, nuclear type 1 | criteria provided, single submitter | research | ||
Revvity Omics, |
RCV000007960 | SCV002023377 | likely pathogenic | Mitochondrial complex 4 deficiency, nuclear type 3 | 2021-05-27 | criteria provided, single submitter | clinical testing | |
Fulgent Genetics, |
RCV000007960 | SCV002776313 | likely pathogenic | Mitochondrial complex 4 deficiency, nuclear type 3 | 2021-07-30 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV003555963 | SCV004296743 | likely pathogenic | not provided | 2024-11-11 | criteria provided, single submitter | clinical testing | This sequence change replaces aspartic acid, which is acidic and polar, with valine, which is neutral and non-polar, at codon 336 of the COX10 protein (p.Asp336Val). This variant is present in population databases (rs104894557, gnomAD 0.02%). This missense change has been observed in individuals with clinical features consistent with mitochondrial complex IV deficiency (PMID: 12928484, 24100867, 32313153). ClinVar contains an entry for this variant (Variation ID: 7525). Invitae Evidence Modeling of protein sequence and biophysical properties (such as structural, functional, and spatial information, amino acid conservation, physicochemical variation, residue mobility, and thermodynamic stability) indicates that this missense variant is expected to disrupt COX10 protein function with a positive predictive value of 80%. Experimental studies have shown that this missense change affects COX10 function (PMID: 22669974, 24100867). In summary, the currently available evidence indicates that the variant is pathogenic, but additional data are needed to prove that conclusively. Therefore, this variant has been classified as Likely Pathogenic. |
Women's Health and Genetics/Laboratory Corporation of America, |
RCV000007960 | SCV005204372 | likely pathogenic | Mitochondrial complex 4 deficiency, nuclear type 3 | 2024-06-12 | criteria provided, single submitter | clinical testing | Variant summary: COX10 c.1007A>T (p.Asp336Val) results in a non-conservative amino acid change in the encoded protein sequence. Five of five in-silico tools predict a damaging effect of the variant on protein function. The variant allele was found at a frequency of 8e-05 in 250112 control chromosomes (gnomAD). This frequency is not significantly higher than estimated for a pathogenic variant in COX10 causing Mitochondrial Complex 4 Deficiency, Nuclear Type 3, allowing no conclusion about variant significance. c.1007A>T has been reported in the literature in compound heterozygous individuals affected with Cytochrome c oxidase deficiency (Antonicka_2003, Riley_2020). These data indicate that the variant may be associated with disease. At least two publications report experimental evidence evaluating an impact on protein function and this variant results in a catalytically inactive enzyme (Khalimonchuk_2012, Pitceathly_2013). The following publications have been ascertained in the context of this evaluation (PMID: 12928484, 22669974, 24100867, 32313153). ClinVar contains an entry for this variant (Variation ID: 7525). Based on the evidence outlined above, the variant was classified as likely pathogenic. |
OMIM | RCV000007960 | SCV000028165 | pathogenic | Mitochondrial complex 4 deficiency, nuclear type 3 | 2003-10-15 | no assertion criteria provided | literature only | |
Johnston Lab, |
RCV003555963 | SCV005200372 | not provided | not provided | no assertion provided | in vitro |