Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000672580 | SCV000797695 | likely pathogenic | Autosomal recessive limb-girdle muscular dystrophy type 2A | 2018-02-06 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV000672580 | SCV002288517 | pathogenic | Autosomal recessive limb-girdle muscular dystrophy type 2A | 2024-11-11 | criteria provided, single submitter | clinical testing | This variant results in the deletion of part of exon 3 (c.380-8_395del) of the CAPN3 gene. It is expected to disrupt RNA splicing. Variants that disrupt the donor or acceptor splice site typically lead to a loss of protein function (PMID: 16199547), and loss-of-function variants in CAPN3 are known to be pathogenic (PMID: 10330340, 15689361). This variant is not present in population databases (gnomAD no frequency). This variant has not been reported in the literature in individuals affected with CAPN3-related conditions. ClinVar contains an entry for this variant (Variation ID: 556559). This variant disrupts a region of the CAPN3 protein in which other variant(s) (p.Trp130Ser) have been determined to be pathogenic (PMID: 33337384). This suggests that this is a clinically significant region of the protein, and that variants that disrupt it are likely to be disease-causing. For these reasons, this variant has been classified as Pathogenic. |