Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Institute of Human Genetics, |
RCV001253279 | SCV001428918 | likely pathogenic | Seizures, benign familial neonatal, 1 | 2017-12-19 | criteria provided, single submitter | clinical testing | |
Ambry Genetics | RCV002430054 | SCV002729363 | pathogenic | Inborn genetic diseases | 2018-06-13 | criteria provided, single submitter | clinical testing | The p.Y363* pathogenic mutation (also known as c.1089C>G), located in coding exon 8 of the KCNQ2 gene, results from a C to G substitution at nucleotide position 1089. This changes the amino acid from a tyrosine to a stop codon within coding exon 8. 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 |
RCV003753169 | SCV004445779 | pathogenic | Early infantile epileptic encephalopathy with suppression bursts | 2023-07-20 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. ClinVar contains an entry for this variant (Variation ID: 976093). This variant has not been reported in the literature in individuals affected with KCNQ2-related conditions. This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Tyr363*) in the KCNQ2 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in KCNQ2 are known to be pathogenic (PMID: 14534157, 23692823, 27779742). |