Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001071877 | SCV001237207 | pathogenic | not provided | 2024-07-08 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Glu671*) in the CNGB3 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in CNGB3 are known to be pathogenic (PMID: 28795510). This variant is present in population databases (rs761969118, gnomAD 0.003%). This variant has not been reported in the literature in individuals affected with CNGB3-related conditions. ClinVar contains an entry for this variant (Variation ID: 864643). For these reasons, this variant has been classified as Pathogenic. |
Institute of Human Genetics, |
RCV004813722 | SCV005068519 | pathogenic | Retinal dystrophy | 2021-01-01 | criteria provided, single submitter | clinical testing | |
Fulgent Genetics, |
RCV005047287 | SCV005679198 | likely pathogenic | Achromatopsia 3 | 2024-02-21 | criteria provided, single submitter | clinical testing | |
Prevention |
RCV004733147 | SCV005348970 | pathogenic | CNGB3-related disorder | 2024-09-09 | no assertion criteria provided | clinical testing | The CNGB3 c.2011G>T variant is predicted to result in premature protein termination (p.Glu671*). To our knowledge, this variant has not been reported in the literature in association with disease. This variant is reported in 0.0035% of alleles in individuals of European (Non-Finnish) descent in gnomAD. Nonsense variants in CNGB3 are an established mechanism of disease. This variant is interpreted as pathogenic. |