Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Ambry Genetics | RCV002424241 | SCV002725893 | pathogenic | Inborn genetic diseases | 2019-03-08 | criteria provided, single submitter | clinical testing | The p.G701* pathogenic mutation (also known as c.2101G>T), located in coding exon 14 of the CNTNAP2 gene, results from a G to T substitution at nucleotide position 2101. This changes the amino acid from a glycine to a stop codon within coding exon 14. This alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. As such, this alteration is interpreted as a disease-causing mutation. |
Labcorp Genetics |
RCV003098614 | SCV003331132 | pathogenic | Cortical dysplasia-focal epilepsy syndrome | 2022-08-08 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. This variant has not been reported in the literature in individuals affected with CNTNAP2-related conditions. This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Gly701*) in the CNTNAP2 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in CNTNAP2 are known to be pathogenic (PMID: 19896112, 21827697, 25045150, 26843181, 27439707). |