Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Laboratory for Molecular Medicine, |
RCV000036067 | SCV000059719 | likely pathogenic | Rare genetic deafness | 2009-06-03 | criteria provided, single submitter | clinical testing | |
Counsyl | RCV000666110 | SCV000790352 | likely pathogenic | Autosomal recessive nonsyndromic hearing loss 2; Usher syndrome type 1 | 2017-03-16 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001852739 | SCV002291582 | likely pathogenic | not provided | 2024-02-16 | criteria provided, single submitter | clinical testing | This sequence change affects an acceptor splice site in intron 2 of the MYO7A 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 MYO7A are known to be pathogenic (PMID: 8900236, 25404053). This variant is not present in population databases (gnomAD no frequency). Disruption of this splice site has been observed in individual(s) with Usher syndrome (PMID: 25468891). ClinVar contains an entry for this variant (Variation ID: 43163). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus splice site. 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. |