Total submissions: 5
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Laboratory for Molecular Medicine, |
RCV000038165 | SCV000061831 | likely benign | not specified | 2012-08-15 | criteria provided, single submitter | clinical testing | Ser494Ser in exon 6 of PKP2: This variant is not expected to have clinical signi ficance because it does not alter an amino acid residue and is not located withi n the splice consensus sequence. Ser494Ser in exon 6 of PKP2 (allele frequency = n/a) |
Invitae | RCV000640036 | SCV000761624 | likely benign | Arrhythmogenic right ventricular dysplasia 9 | 2024-01-17 | criteria provided, single submitter | clinical testing | |
Color Diagnostics, |
RCV001183719 | SCV001349529 | likely benign | Cardiomyopathy | 2020-01-10 | criteria provided, single submitter | clinical testing | |
Ambry Genetics | RCV003162331 | SCV003866156 | uncertain significance | Cardiovascular phenotype | 2023-01-05 | criteria provided, single submitter | clinical testing | The c.1482A>G variant (also known as p.S494S), located in coding exon 6 of the PKP2 gene, results from an A to G substitution at nucleotide position 1482. This nucleotide substitution does not change the serine at codon 494. This nucleotide position is highly conserved in available vertebrate species. In silico splice site analysis for this alteration is inconclusive. In addition, coding exon 6 is alternatively spliced, and the predominant isoform in human cardiac tissue, PKP2A, does not include this exon (Gandjbakhch E et al. Heart. 2011;97(10):844-9). Since supporting evidence is limited at this time, the clinical significance of this alteration remains unclear. |
All of Us Research Program, |
RCV003996368 | SCV004846389 | likely benign | Arrhythmogenic right ventricular cardiomyopathy | 2023-11-20 | criteria provided, single submitter | clinical testing |