Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000169174 | SCV000220405 | likely pathogenic | Achromatopsia 3 | 2014-06-11 | criteria provided, single submitter | literature only | |
Molecular Genetics Laboratory, |
RCV000596854 | SCV000700209 | pathogenic | Achromatopsia | 2018-03-20 | criteria provided, single submitter | research | |
Labcorp Genetics |
RCV001380986 | SCV001579229 | pathogenic | not provided | 2022-12-18 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Gln38*) 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 not present in population databases (gnomAD no frequency). This premature translational stop signal has been observed in individual(s) with achrompatopsia (PMID: 15657609, 28795510, 30418171). In at least one individual the data is consistent with being in trans (on the opposite chromosome) from a pathogenic variant. ClinVar contains an entry for this variant (Variation ID: 188828). For these reasons, this variant has been classified as Pathogenic. |
Molecular Genetics Laboratory, |
RCV000169174 | SCV000575819 | pathogenic | Achromatopsia 3 | 2017-03-27 | no assertion criteria provided | research |