Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000487191 | SCV000573441 | likely pathogenic | not provided | 2024-10-14 | criteria provided, single submitter | clinical testing | Frameshift 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); Has not been previously published as pathogenic or benign to our knowledge |
Baylor Genetics | RCV004568212 | SCV005052587 | likely pathogenic | Myopathy, lactic acidosis, and sideroblastic anemia 1 | 2023-11-30 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV000487191 | SCV005706426 | pathogenic | not provided | 2024-03-13 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Ala152Glyfs*13) in the PUS1 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in PUS1 are known to be pathogenic (PMID: 17056637, 19731322, 25058219, 26556812). This variant is not present in population databases (gnomAD no frequency). This variant has not been reported in the literature in individuals affected with PUS1-related conditions. ClinVar contains an entry for this variant (Variation ID: 423712). For these reasons, this variant has been classified as Pathogenic. |
Natera, |
RCV001829384 | SCV002091058 | likely pathogenic | Myopathy, lactic acidosis, and sideroblastic anemia | 2017-06-26 | no assertion criteria provided | clinical testing |