Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Genetic Services Laboratory, |
RCV000193685 | SCV000249327 | pathogenic | Microcephaly and chorioretinopathy with or without intellectual disability | 2014-12-12 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001853120 | SCV002137372 | pathogenic | not provided | 2022-06-08 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg299*) in the TUBGCP6 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in TUBGCP6 are known to be pathogenic (PMID: 25344692). This variant is present in population databases (rs192919234, gnomAD 0.03%). This variant has not been reported in the literature in individuals affected with TUBGCP6-related conditions. ClinVar contains an entry for this variant (Variation ID: 212517). 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. |
DASA | RCV002298518 | SCV002588778 | pathogenic | Microcephaly and chorioretinopathy 1 | 2022-11-03 | criteria provided, single submitter | clinical testing | The c.895C>T;p.(Arg299*) variant creates a premature translational stop signal in the TUBGCP6 gene. It is expected to result in an absent or disrupted protein product - PVS1. ClinVar contains an entry for this variant (Clinvar ID:212517) - PS4_supporting. The variant is present at low allele frequencies population databases (rs192919234 – gnomAD 0.0002127%; ABraOM 0.000427 frequency - https://abraom.ib.usp.br/) - PM2_supporting. In summary, the currently available evidence indicates that the variant is pathogenic. |