Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Athena Diagnostics | RCV000711237 | SCV000841569 | likely pathogenic | not provided | 2017-12-29 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001861960 | SCV002235743 | pathogenic | Congenital myotonia, autosomal recessive form; Congenital myotonia, autosomal dominant form | 2022-10-25 | criteria provided, single submitter | clinical testing | Advanced modeling of protein sequence and biophysical properties (such as structural, functional, and spatial information, amino acid conservation, physicochemical variation, residue mobility, and thermodynamic stability) performed at Invitae indicates that this missense variant is expected to disrupt CLCN1 protein function. For these reasons, this variant has been classified as Pathogenic. This variant disrupts the p.Leu198 amino acid residue in CLCN1. Other variant(s) that disrupt this residue have been determined to be pathogenic (PMID: 15241802, 23113340; Invitae). This suggests that this residue is clinically significant, and that variants that disrupt this residue are likely to be disease-causing. Experimental studies have shown that this missense change affects CLCN1 function (PMID: 26096614). ClinVar contains an entry for this variant (Variation ID: 585692). This missense change has been observed in individuals with autosomal dominant myotonia congenita (PMID: 23483815, 26096614). This variant is not present in population databases (gnomAD no frequency). This sequence change replaces leucine, which is neutral and non-polar, with proline, which is neutral and non-polar, at codon 198 of the CLCN1 protein (p.Leu198Pro). |