Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000598791 | SCV000710485 | pathogenic | not provided | 2018-02-02 | criteria provided, single submitter | clinical testing | The Q112X variant in the ROGDI gene has not been reported previously as a pathogenic variant nor as a benign variant, to our knowledge. This variant is predicted to cause loss of normal protein function either through protein truncation or nonsense-mediated mRNA decay. The Q112X variant is not observed at a significant frequency in large population cohorts (Lek et al., 2016). We interpret Q112X as a pathogenic variant. |
Labcorp Genetics |
RCV001213867 | SCV001385519 | pathogenic | Amelocerebrohypohidrotic syndrome | 2019-10-16 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. Loss-of-function variants in ROGDI are known to be pathogenic (PMID: 22424600, 23086778). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may create or strengthen a splice site, but this prediction has not been confirmed by published transcriptional studies. This variant has not been reported in the literature in individuals with ROGDI-related conditions. ClinVar contains an entry for this variant (Variation ID: 504177). This variant is present in population databases (rs372097881, ExAC 0.04%). This sequence change creates a premature translational stop signal (p.Gln112*) in the ROGDI gene. It is expected to result in an absent or disrupted protein product. |
Fulgent Genetics, |
RCV001213867 | SCV005646916 | likely pathogenic | Amelocerebrohypohidrotic syndrome | 2024-05-30 | criteria provided, single submitter | clinical testing |