Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV003074949 | SCV003460070 | pathogenic | Aniridia 1; Irido-corneo-trabecular dysgenesis | 2022-08-22 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. This variant disrupts the p.Arg38 amino acid residue in PAX6. Other variant(s) that disrupt this residue have been determined to be pathogenic (PMID: 29145603, 34415986). This suggests that this residue is clinically significant, and that variants that disrupt this residue are likely to be disease-causing. 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 PAX6 protein function. This missense change has been observed in individual(s) with clinical features of autosomal dominant aniridia (PMID: 29914532, 31700164). It has also been observed to segregate with disease in related individuals. This variant is not present in population databases (gnomAD no frequency). This sequence change replaces arginine, which is basic and polar, with glutamine, which is neutral and polar, at codon 38 of the PAX6 protein (p.Arg38Gln). |
Molecular Medicine, |
RCV003491223 | SCV004023260 | likely pathogenic | Irido-corneo-trabecular dysgenesis | 2023-07-28 | criteria provided, single submitter | research | |
OMIM | RCV003883472 | SCV004697968 | pathogenic | Coloboma, ocular, autosomal dominant | 2024-03-01 | no assertion criteria provided | literature only |