Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001305693 | SCV001495039 | likely pathogenic | GLUT1 deficiency syndrome 1, autosomal recessive | 2023-06-14 | criteria provided, single submitter | clinical testing | In summary, the currently available evidence indicates that the variant is pathogenic, but additional data are needed to prove that conclusively. Therefore, this variant has been classified as Likely Pathogenic. 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 SLC2A1 protein function. ClinVar contains an entry for this variant (Variation ID: 1008366). This missense change has been observed in individual(s) with clinical features of autosomal dominant glucose transporter type 1 deficiency syndrome (Invitae). This variant is not present in population databases (gnomAD no frequency). This sequence change replaces alanine, which is neutral and non-polar, with valine, which is neutral and non-polar, at codon 301 of the SLC2A1 protein (p.Ala301Val). |
3billion | RCV001779153 | SCV002014693 | uncertain significance | Encephalopathy due to GLUT1 deficiency | 2021-10-25 | criteria provided, single submitter | clinical testing | This variant is not observed in the gnomAD v2.1.1 dataset (PM2). In silico tool predictions suggest damaging effect of the variant on gene or gene product (REVEL: 0.685, PP3). Therefore, this variant is classified as uncertain significance according to the recommendation of ACMG/AMP guideline. |