Total submissions: 1
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001995963 | SCV002272932 | likely pathogenic | Heterotopia, periventricular, X-linked dominant; Melnick-Needles syndrome; Oto-palato-digital syndrome, type II; Frontometaphyseal dysplasia | 2021-10-24 | criteria provided, single submitter | clinical testing | Studies have shown that this premature translational stop signal alters FLNA gene expression (PMID: 26059841). 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. Studies have shown that this premature translational stop signal results in skipping of exon 39 (also known as exon 40), but is expected to preserve the integrity of the reading-frame (PMID: 26059841). This variant is also known as c.6425_6428delAGAG (p.Glu2142Alafs*22). This premature translational stop signal has been observed in individual(s) with chronic idiopathic intestinal pseudo-obstruction (PMID: 26059841). This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Glu2134Alafs*22) in the FLNA gene. RNA analysis indicates that this premature translational stop signal induces altered splicing and likely results in a shortened protein product. |