Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV001008934 | SCV001168741 | likely pathogenic | not provided | 2018-07-10 | criteria provided, single submitter | clinical testing | The c.2017_2018delGC variant is not observed in large population cohorts (Lek et al., 2016). The c.2017_2018delGC variant causes a frameshift starting with codon Alanine 673, changes this amino acid to a Serine residue, and creates a premature Stop codon at position 40 of the new reading frame, denoted p.Ala673SerfsX40. This variant is predicted to cause loss of normal protein function either through protein truncation or nonsense-mediated mRNA decay. Although the c.2017_2018delGC variant has not been reported previously to our knowledge, other loss-of-function variants in the CLCN1 gene have been reported in the Human Gene Mutation Database in association with CLCN1-related disorders (Stenson et al., 2014). |
Labcorp Genetics |
RCV001035266 | SCV001198589 | pathogenic | Congenital myotonia, autosomal recessive form; Congenital myotonia, autosomal dominant form | 2019-03-07 | criteria provided, single submitter | clinical testing | This variant is not present in population databases (ExAC no frequency). This sequence change creates a premature translational stop signal (p.Ala673Serfs*40) in the CLCN1 gene. It is expected to result in an absent or disrupted protein product. This variant has not been reported in the literature in individuals with CLCN1-related conditions. For these reasons, this variant has been classified as Pathogenic. Loss-of-function variants in CLCN1 are known to be pathogenic (PMID: 17932099, 22094069, 23739125). |