Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001863711 | SCV002121709 | pathogenic | Congenital myotonia, autosomal recessive form; Congenital myotonia, autosomal dominant form | 2022-06-20 | criteria provided, single submitter | clinical testing | This variant has not been reported in the literature in individuals affected with CLCN1-related conditions. This sequence change creates a premature translational stop signal (p.Glu717Argfs*80) in the CLCN1 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in CLCN1 are known to be pathogenic (PMID: 17932099, 22094069, 23739125). This variant is not present in population databases (gnomAD no frequency). For these reasons, this variant has been classified as Pathogenic. |
3billion, |
RCV002283563 | SCV002572668 | pathogenic | Congenital myotonia, autosomal recessive form | 2022-09-01 | criteria provided, single submitter | clinical testing | The variant is not observed in the gnomAD v2.1.1 dataset. Frameshift variant is predicted to result in a loss or disruption of normal protein function through nonsense-mediated decay (NMD) or protein truncation. Multiple pathogenic variants are reported downstream of the variant. The variant is in trans with the other variant. The variant has been reported to be associated with CLCN1-related disorder (ClinVar ID: VCV001354004). Therefore, this variant is classified as Pathogenic according to the recommendation of ACMG/AMP guideline. |