Total submissions: 1
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV000541059 | SCV000626798 | likely pathogenic | Ornithine aminotransferase deficiency | 2016-09-15 | criteria provided, single submitter | clinical testing | This sequence change deletes 9 nucleotides and inserts 5 nucleotides in exon 2 of the OAT mRNA (c.198_199+7delinsTTAAT). It affects the donor splice site in intron 2 of the OAT gene. It is expected to disrupt mRNA splicing and likely results in an absent or disrupted protein product. In summary, donor and acceptor splice site variants are typically loss-of-function (PMID: 16199547), and loss-of-function variants in OAT are known to be pathogenic (PMID: 23076989). However, without additional functional and/or genetic data, this variant has been classified as Likely Pathogenic. This variant has not been reported in the literature in individuals with a OAT-related disease. |