Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001854500 | SCV002304183 | pathogenic | Leber congenital amaurosis 7; Cone-rod dystrophy 2 | 2022-06-09 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. This variant disrupts the p.Glu80 amino acid residue in CRX. Other variant(s) that disrupt this residue have been determined to be pathogenic (PMID: 9390563, 11971869). This suggests that this residue is clinically significant, and that variants that disrupt this residue are likely to be disease-causing. Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus splice site. Algorithms developed to predict the effect of missense changes on protein structure and function (SIFT, PolyPhen-2, Align-GVGD) all suggest that this variant is likely to be disruptive. ClinVar contains an entry for this variant (Variation ID: 99599). This missense change has been observed in individuals with clinical features of autosomal dominant inherited retinal dystrophy (PMID: 10874321, 33691693; Invitae). This variant is not present in population databases (gnomAD no frequency). This sequence change replaces glutamic acid, which is acidic and polar, with lysine, which is basic and polar, at codon 80 of the CRX protein (p.Glu80Lys). |
Retina International | RCV000085994 | SCV000118137 | not provided | not provided | no assertion provided | not provided | ||
Sharon lab, |
RCV001003002 | SCV001161056 | likely pathogenic | maculopathy | 2019-06-23 | no assertion criteria provided | research |