Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV003539023 | SCV004284891 | pathogenic | Peroxisome biogenesis disorder 11A (Zellweger) | 2022-11-02 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. This premature translational stop signal has been observed in individual(s) with PEX13-related conditions (PMID: 21031596). This variant is present in population databases (rs146554084, gnomAD 0.007%). This sequence change creates a premature translational stop signal (p.Arg226*) in the PEX13 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in PEX13 are known to be pathogenic (PMID: 10332040, 21031596). |
Prevention |
RCV004554253 | SCV004712986 | pathogenic | PEX13-related disorder | 2023-12-18 | no assertion criteria provided | clinical testing | The PEX13 c.676C>T variant is predicted to result in premature protein termination (p.Arg226*). This variant has been reported in the homozygous state in individuals with Zellweger syndrome H (Ebberink et al 2011. PubMed ID: 21031596). This variant is reported in 0.0062% of alleles in individuals of African descent in gnomAD. Nonsense variants in PEX13 are expected to be pathogenic. This variant is interpreted as pathogenic. |