Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000331831 | SCV000330583 | pathogenic | not provided | 2019-12-30 | 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; Has not been previously published as pathogenic or benign to our knowledge |
Institute of Medical Genetics and Applied Genomics, |
RCV000331831 | SCV001447533 | pathogenic | not provided | 2020-10-23 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV002519061 | SCV003240989 | pathogenic | Creatine transporter deficiency | 2022-03-18 | criteria provided, single submitter | clinical testing | 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. ClinVar contains an entry for this variant (Variation ID: 280650). This sequence change creates a premature translational stop signal (p.Asp431Leufs*27) in the SLC6A8 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in SLC6A8 are known to be pathogenic (PMID: 22281021). This variant is not present in population databases (gnomAD no frequency). This variant has not been reported in the literature in individuals affected with SLC6A8-related conditions. |