Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000481165 | SCV000566472 | pathogenic | not provided | 2015-05-07 | criteria provided, single submitter | clinical testing | The c.391delC deletion in the SGCA gene causes a frameshift starting with codon Leucine 131, changes thisamino acid to a Cysteine residue and creates a premature Stop codon at position 80 of the new reading frame,denoted p.Leu131CysfsX80. This variant is predicted to cause loss of normal protein function either throughprotein truncation or nonsense-mediated mRNA decay. Therefore, we interpret the c.391delC as a pathogenic variant. |
Labcorp Genetics |
RCV000536997 | SCV000649769 | pathogenic | Autosomal recessive limb-girdle muscular dystrophy type 2D | 2022-08-15 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. ClinVar contains an entry for this variant (Variation ID: 418990). This variant has not been reported in the literature in individuals affected with SGCA-related conditions. This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Leu131Cysfs*80) in the SGCA gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in SGCA are known to be pathogenic (PMID: 9192266). |
Genome- |
RCV000536997 | SCV003931665 | pathogenic | Autosomal recessive limb-girdle muscular dystrophy type 2D | 2023-02-08 | criteria provided, single submitter | clinical testing |