Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Revvity Omics, |
RCV001781161 | SCV002021743 | pathogenic | not provided | 2023-05-17 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001851535 | SCV002142921 | pathogenic | Fetal akinesia deformation sequence 1; Congenital myasthenic syndrome 10 | 2023-10-20 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg201*) in the DOK7 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in DOK7 are known to be pathogenic (PMID: 16794080, 16917026, 18626973, 19261599). This variant is present in population databases (rs118203995, gnomAD 0.003%). This premature translational stop signal has been observed in individuals with congenital myasthenic syndrome (PMID: 16917026, 25849006). ClinVar contains an entry for this variant (Variation ID: 1279). Algorithms developed to predict the effect of variants on protein structure and function are not available or were not evaluated for this variant. Experimental studies have shown that this premature translational stop signal affects DOK7 function (PMID: 18165682). For these reasons, this variant has been classified as Pathogenic. |
Baylor Genetics | RCV004566668 | SCV005059601 | pathogenic | Fetal akinesia deformation sequence 3 | 2023-12-10 | criteria provided, single submitter | clinical testing | |
OMIM | RCV000001341 | SCV000021491 | pathogenic | Congenital myasthenic syndrome 10 | 2006-09-29 | no assertion criteria provided | literature only |