Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000782124 | SCV000854633 | pathogenic | Delayed gross motor development | 2018-07-30 | criteria provided, single submitter | clinical testing | |
Fulgent Genetics, |
RCV002499389 | SCV002809526 | pathogenic | COG4-congenital disorder of glycosylation; Microcephalic osteodysplastic dysplasia, Saul-Wilson type | 2022-03-29 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV003609168 | SCV004512843 | pathogenic | COG4-congenital disorder of glycosylation | 2023-11-28 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Glu614*) in the COG4 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in COG4 are known to be pathogenic (PMID: 21185756). This variant is present in population databases (no rsID available, gnomAD 0.007%). This premature translational stop signal has been observed in individual(s) with congenital disorder of glycosylation (PMID: 32064623). ClinVar contains an entry for this variant (Variation ID: 599648). For these reasons, this variant has been classified as Pathogenic. |
Gene |
RCV000760680 | SCV000890572 | pathogenic | not provided | 2020-09-29 | flagged submission | clinical testing | The E614X variant in the COG4 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 E614X variant is not observed at a significant frequency in large population cohorts (Lek et al., 2016). We interpret E614X as a pathogenic variant. |