Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Mendelics | RCV002250070 | SCV002516615 | pathogenic | Progressive myoclonic epilepsy type 3 | 2022-05-04 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV002250070 | SCV003508263 | uncertain significance | Progressive myoclonic epilepsy type 3 | 2022-06-02 | criteria provided, single submitter | clinical testing | In summary, the available evidence is currently insufficient to determine the role of this variant in disease. Therefore, it has been classified as a Variant of Uncertain Significance. This variant disrupts the p.Arg94 amino acid residue in KCTD7. Other variant(s) that disrupt this residue have been determined to be pathogenic (PMID: 22606975, 22693283, 27742667, 34866617). This suggests that this residue is clinically significant, and that variants that disrupt this residue are likely to be disease-causing. Algorithms developed to predict the effect of missense changes on protein structure and function are either unavailable or do not agree on the potential impact of this missense change (SIFT: "Deleterious"; PolyPhen-2: "Probably Damaging"; Align-GVGD: "Class C0"). This variant has not been reported in the literature in individuals affected with KCTD7-related conditions. This variant is present in population databases (no rsID available, gnomAD 0.007%). This sequence change replaces arginine, which is basic and polar, with glutamine, which is neutral and polar, at codon 94 of the KCTD7 protein (p.Arg94Gln). |