Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Institute of Human Genetics, |
RCV001706856 | SCV001934396 | likely pathogenic | Intellectual disability, autosomal dominant 42 | 2021-01-19 | criteria provided, single submitter | clinical testing | This variant was identified as de novo (maternity and paternity confirmed). |
Labcorp Genetics |
RCV002300570 | SCV002589231 | uncertain significance | not provided | 2022-10-03 | criteria provided, single submitter | clinical testing | In summary, the available evidence is currently insufficient to determine the role of this variant in disease. Therefore, it has been classified as a Variant of Uncertain Significance. Advanced modeling of protein sequence and biophysical properties (such as structural, functional, and spatial information, amino acid conservation, physicochemical variation, residue mobility, and thermodynamic stability) performed at Invitae indicates that this missense variant is expected to disrupt GNB1 protein function. ClinVar contains an entry for this variant (Variation ID: 1285499). This variant has not been reported in the literature in individuals affected with GNB1-related conditions. This variant is not present in population databases (gnomAD no frequency). This sequence change replaces aspartic acid, which is acidic and polar, with asparagine, which is neutral and polar, at codon 163 of the GNB1 protein (p.Asp163Asn). |