Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000409821 | SCV000486310 | likely pathogenic | Cohen syndrome | 2016-05-09 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV000409821 | SCV002278875 | likely pathogenic | Cohen syndrome | 2021-06-02 | criteria provided, single submitter | clinical testing | This variant is not present in population databases (ExAC no frequency). In summary, the currently available evidence indicates that the variant is pathogenic, but additional data are needed to prove that conclusively. Therefore, this variant has been classified as Likely Pathogenic. Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus 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 VPS13B-related conditions. ClinVar contains an entry for this variant (Variation ID: 370883). This sequence change affects a donor splice site in intron 39 of the VPS13B gene. It is expected to disrupt RNA splicing. Variants that disrupt the donor or acceptor splice site typically lead to a loss of protein function (PMID: 16199547), and loss-of-function variants in VPS13B are known to be pathogenic (PMID: 15141358, 16648375, 20461111). |