Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Revvity Omics, |
RCV001782348 | SCV002016814 | likely pathogenic | Nemaline myopathy 9 | 2021-02-06 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001782348 | SCV002245683 | pathogenic | Nemaline myopathy 9 | 2024-05-02 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Gly473Argfs*22) in the KLHL41 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in KLHL41 are known to be pathogenic (PMID: 24268659). This variant is present in population databases (rs749464576, gnomAD 0.005%). This variant has not been reported in the literature in individuals affected with KLHL41-related conditions. ClinVar contains an entry for this variant (Variation ID: 1324628). For these reasons, this variant has been classified as Pathogenic. |
Prevention |
RCV003892845 | SCV004714667 | likely pathogenic | KLHL41-related disorder | 2023-12-19 | no assertion criteria provided | clinical testing | The KLHL41 c.1416dupA variant is predicted to result in a frameshift and premature protein termination (p.Gly473Argfs*22). To our knowledge, this variant has not been reported in the literature. This variant is reported in 0.0054% of alleles in individuals of European (Non-Finnish) descent in gnomAD. Frameshift variants in KLHL41 are expected to be pathogenic. This variant is interpreted as likely pathogenic. |