Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Department Of Genetics, |
RCV000761494 | SCV000891613 | pathogenic | Knobloch syndrome | 2017-12-30 | criteria provided, single submitter | curation | |
Centogene AG - |
RCV000761494 | SCV001426509 | pathogenic | Knobloch syndrome | criteria provided, single submitter | clinical testing | ||
DASA | RCV000761494 | SCV002061249 | pathogenic | Knobloch syndrome | 2022-01-05 | criteria provided, single submitter | clinical testing | The c.3509_3518del;p.(Pro1170Leufs*35) is a null frameshift variant (NMD) in the COL18A1 gene and predicts alteration of the nonsense-mediate decay - NMD is present in a relevantexon to the transcript -PVS1. This sequence change has been observed in affected individual(s) and ClinVar contains an entry for this variant (PMID: 32860008) - PS4. This variant is not present in population databases (rs756797124, gnomAD; ABraOM no frequency - http://abraom.ib.usp.br/) - PM2. The p.(Pro1170Leufs*35) was detected in trans with a pathogenic variant (PMID: 32860008) -PM3. In summary, the currently available evidence indicates that the variant is pathogenic. |
Labcorp Genetics |
RCV001855942 | SCV002184569 | pathogenic | not provided | 2023-12-11 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Pro990Leufs*35) in the COL18A1 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in COL18A1 are known to be pathogenic (PMID: 12415512, 25456301). This variant is present in population databases (rs756797124, gnomAD 0.002%). This premature translational stop signal has been observed in individuals with clinical features of Knobloch syndrome (PMID: 12415512, 32860008). ClinVar contains an entry for this variant (Variation ID: 623349). For these reasons, this variant has been classified as Pathogenic. |