Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Color Diagnostics, |
RCV001843273 | SCV001352351 | pathogenic | Cardiac arrhythmia | 2020-03-20 | criteria provided, single submitter | clinical testing | This variant changes 1 nucleotide in exon 2 of the SCN5A gene, creating a premature translation stop signal. This variant is expected to result in an absent or non-functional protein product. To our knowledge, functional assays have not been performed for this variant. This variant has been reported in an individual affected with Brugada syndrome (PMID: 22840528). This variant has not been identified in the general population by the Genome Aggregation Database (gnomAD). Loss of SCN5A function is a known mechanism of disease. Based on available evidence, this variant is classified as Pathogenic. |
New York Genome Center | RCV002265957 | SCV002548570 | pathogenic | Brugada syndrome 1; Long QT syndrome 3 | 2021-07-02 | criteria provided, single submitter | clinical testing | The heterozygous nonsense variant c.127C>T, p.Arg43Ter in exon 2 of the SCN5A gene, creates a premature translation stop signal at AA 43. This variant isexpected to result in an absent or non-functional protein product. This variant has been reported in an individual affected with Brugada syndrome (PMID:22840528). The variant is absent in the gnomAD v3.1.1 database, suggesting it is not a common benign variant in the populations represented in this database. Loss of function is a known mechanism of SCN5A associated Brugada syndrome. Based on available evidence, this variant is classified as Pathogenic. |