Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV000662358 | SCV001228264 | pathogenic | Myasthenic syndrome, congenital, 22 | 2023-10-17 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg295*) in the PREPL gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in PREPL are known to be pathogenic (PMID: 24610330, 28726805, 29913539). This variant is present in population databases (rs145356495, gnomAD 0.01%). This premature translational stop signal has been observed in individual(s) with PREPL deficiency (PMID: 28726805). ClinVar contains an entry for this variant (Variation ID: 548713). For these reasons, this variant has been classified as Pathogenic. |
Gene |
RCV002285394 | SCV002575479 | likely pathogenic | not provided | 2022-03-23 | criteria provided, single submitter | clinical testing | Identified heterozygous in a patient with features consistent with PREPL deficiency who also harbored a heterozygous deletion involving PREPL and CAMKMT, however, familial segregation information was not provided (Regal et al., 2018); 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: 31985178, 32721234, 28726805) |
OMIM | RCV000662358 | SCV000784721 | pathogenic | Myasthenic syndrome, congenital, 22 | 2018-07-11 | no assertion criteria provided | literature only |