Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000439368 | SCV000514258 | pathogenic | not provided | 2022-08-27 | criteria provided, single submitter | clinical testing | 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: 29175898) |
Baylor Genetics | RCV003476014 | SCV004204090 | pathogenic | Muscular dystrophy-dystroglycanopathy (congenital with brain and eye anomalies), type A2 | 2024-02-29 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV003766201 | SCV004569491 | pathogenic | Muscular dystrophy-dystroglycanopathy (congenital with brain and eye anomalies), type A2; Muscular dystrophy-dystroglycanopathy (congenital with intellectual disability), type B2; Autosomal recessive limb-girdle muscular dystrophy type 2N | 2023-12-11 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg588*) in the POMT2 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in POMT2 are known to be pathogenic (PMID: 15894594). This variant is present in population databases (rs766169193, gnomAD 0.003%). This premature translational stop signal has been observed in individual(s) with limb-girdle muscular dystrophy (PMID: 29175898). ClinVar contains an entry for this variant (Variation ID: 378419). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus splice site. For these reasons, this variant has been classified as Pathogenic. |