Total submissions: 5
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV000550931 | SCV000659878 | pathogenic | RYR1-related disorder | 2023-01-28 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Gln677*) in the RYR1 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in RYR1 are known to be pathogenic (PMID: 20583297, 20839240, 23919265, 28818389). This variant is present in population databases (no rsID available, gnomAD 0.0009%). This premature translational stop signal has been observed in individual(s) with congenital muscular dystrophy (PMID: 27854218). ClinVar contains an entry for this variant (Variation ID: 242414). For these reasons, this variant has been classified as Pathogenic. |
Revvity Omics, |
RCV001782728 | SCV002019940 | pathogenic | not provided | 2020-06-24 | criteria provided, single submitter | clinical testing | |
Fulgent Genetics, |
RCV005003587 | SCV002780224 | pathogenic | Central core myopathy; Malignant hyperthermia, susceptibility to, 1; Congenital multicore myopathy with external ophthalmoplegia; King Denborough syndrome | 2024-06-19 | criteria provided, single submitter | clinical testing | |
Gene |
RCV001782728 | SCV005201363 | pathogenic | not provided | 2023-12-21 | criteria provided, single submitter | clinical testing | Observed with another RYR1 variant in an individual with congenital muscular dystrophy in published literature (PMID: 27854218); Nonsense variant predicted to result in protein truncation or nonsense mediated decay in a gene for which loss of function is a known mechanism of disease; Not observed at significant frequency in large population cohorts (gnomAD); This variant is associated with the following publications: (PMID: 27854218) |
Prevention |
RCV000550931 | SCV004118588 | pathogenic | RYR1-related disorder | 2024-01-31 | no assertion criteria provided | clinical testing | The RYR1 c.2029C>T variant is predicted to result in premature protein termination (p.Gln677*). This variant, along with a missense variant in RYR1, were reported in the compound heterozygous state in an individual with congenital muscular dystrophy (#11, Punetha et al. 2016. PubMed ID: 27854218). This variant is reported in one allele out of ~251,000 alleles in the gnomAD database. Loss of function variants, including frameshift, splicing, and nonsense variants have only been observed for the autosomal recessive myopathy phenotype and are expected to be pathogenic for this phenotype. Loss of function variants are not established for autosomal dominant malignant hyperthermia. Taken together, this variant is interpreted as pathogenic for autosomal recessive RYR1-related disorders and interpreted as uncertain for autosomal dominant malignant hyperthermia. |