Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001223167 | SCV001395303 | pathogenic | Combined oxidative phosphorylation defect type 17 | 2023-12-11 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Glu30*) in the ELAC2 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in ELAC2 are known to be pathogenic (PMID: 27769300, 31045291). This variant is present in population databases (rs767879725, gnomAD 0.03%). This variant has not been reported in the literature in individuals affected with ELAC2-related conditions. ClinVar contains an entry for this variant (Variation ID: 951292). For these reasons, this variant has been classified as Pathogenic. |
Gene |
RCV001223167 | SCV002011824 | pathogenic | Combined oxidative phosphorylation defect type 17 | 2019-05-08 | criteria provided, single submitter | clinical testing | This variant results in an amino acid alteration, replacing a glutamic acid (E) with a premature stop codon at position 30 noted as p.Glu30Ter or p.E30*. The substitution is predicted to result in a non-functional protein, either through protein truncation or nonsense-mediated mRNA decay. This variant is considered a non-tolerated amino acid change based on “in silico” prediction algorithms (disease causing), and it has been reported in the gnomAD database at a frequency of 0.000058.Based on these findings and the limited literature regarding this substitution we consider it as a “likely pathogenic variant”. |
Mayo Clinic Laboratories, |
RCV003481003 | SCV004226907 | likely pathogenic | not provided | 2023-01-17 | criteria provided, single submitter | clinical testing | PVS1 |