Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Institute of Human Genetics, |
RCV000019952 | SCV001934390 | likely pathogenic | Congenital myopathy with fiber type disproportion | 2021-01-12 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001851954 | SCV002226844 | uncertain significance | Actin accumulation myopathy | 2022-09-13 | criteria provided, single submitter | clinical testing | This sequence change replaces leucine, which is neutral and non-polar, with proline, which is neutral and non-polar, at codon 223 of the ACTA1 protein (p.Leu223Pro). In summary, the available evidence is currently insufficient to determine the role of this variant in disease. Therefore, it has been classified as a Variant of Uncertain Significance. Experimental studies have shown that this missense change affects ACTA1 function (PMID: 19206168). 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 not expected to disrupt ACTA1 protein function. ClinVar contains an entry for this variant (Variation ID: 18290). This variant is also known as p.Leu221Pro. This missense change has been observed in individual(s) with congenital fibre type disproportion (PMID: 15468086). This variant is not present in population databases (gnomAD no frequency). |
OMIM | RCV003151735 | SCV000040250 | pathogenic | Congenital myopathy 2c, severe infantile, autosomal dominant | 2004-11-01 | no assertion criteria provided | literature only | |
Gene |
RCV000019952 | SCV000058544 | not provided | Congenital myopathy with fiber type disproportion | no assertion provided | literature only |