Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001994497 | SCV002234173 | pathogenic | Early infantile epileptic encephalopathy with suppression bursts | 2022-06-24 | 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 ST3GAL3-related conditions. This variant is present in population databases (no rsID available, gnomAD 0.003%). This sequence change creates a premature translational stop signal (p.Arg261*) in the ST3GAL3 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in ST3GAL3 are known to be pathogenic (PMID: 31584066). |
Ambry Genetics | RCV002407174 | SCV002670810 | pathogenic | Inborn genetic diseases | 2018-03-09 | criteria provided, single submitter | clinical testing | The p.R261* pathogenic mutation (also known as c.781C>T), located in coding exon 9 of the ST3GAL3 gene, results from a C to T substitution at nucleotide position 781. This changes the amino acid from an arginine to a stop codon within coding exon 9. 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. |
Center for Genomics, |
RCV003224596 | SCV003920509 | pathogenic | Intellectual disability, autosomal recessive 12; Developmental and epileptic encephalopathy, 15 | 2022-12-05 | criteria provided, single submitter | clinical testing | This variant has not been reported in the literature but is present in the Genome Aggregation Database (Highest reported MAF 0.001% (1/68000) (https://gnomad.broadinstitute.org/variant/1-43920440-C-T?dataset=gnomad_r3). This variant is present in ClinVar (Variation ID:1452219). Evolutionary conservation and computational predictive tools for this variant are limited or unavailable. This variant creates a premature stop at this codon which results in an absent or abnormal protein. Loss of function variants have been reported in association with disease for this gene (Indellicato 2020 PMID:31584066). In summary, data on this variant is highly suspicious for disease, but requires further evidence for pathogenicity. Therefore, this variant is classified as likely pathogenic. |