Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001350386 | SCV001544783 | pathogenic | Retinitis pigmentosa 12; Leber congenital amaurosis 8 | 2024-04-08 | criteria provided, single submitter | clinical testing | This sequence change replaces cysteine, which is neutral and slightly polar, with serine, which is neutral and polar, at codon 1229 of the CRB1 protein (p.Cys1229Ser). This variant is present in population databases (no rsID available, gnomAD 0.002%). This missense change has been observed in individuals with clinical features of CRB1-related conditions (PMID: 25474345; Invitae). ClinVar contains an entry for this variant (Variation ID: 1045903). 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 CRB1 protein function with a positive predictive value of 95%. For these reasons, this variant has been classified as Pathogenic. |
Baylor Genetics | RCV003473873 | SCV004211152 | likely pathogenic | Leber congenital amaurosis 8 | 2023-08-24 | criteria provided, single submitter | clinical testing | |
Fulgent Genetics, |
RCV005005862 | SCV005637078 | likely pathogenic | Pigmented paravenous retinochoroidal atrophy; Retinitis pigmentosa 12; Leber congenital amaurosis 8 | 2024-01-30 | criteria provided, single submitter | clinical testing | |
Prevention |
RCV004740672 | SCV005346079 | uncertain significance | CRB1-related disorder | 2024-07-26 | no assertion criteria provided | clinical testing | The CRB1 c.3686G>C variant is predicted to result in the amino acid substitution p.Cys1229Ser. This variant has been reported in the compound heterozygous state in an individual with Stargardt macular dystrophy (Zaneveld et al. 2015. PubMed ID: 25474345). This variant is reported in 0.0018% of alleles in individuals of European (Non-Finnish) descent in gnomAD. Missense prediction programs classify this amino acid change as damaging; however, no functional studies have been performed to confirm this. Although we suspect that this variant may be pathogenic, at this time, the clinical significance of this variant is uncertain due to the absence of conclusive functional and genetic evidence. |