Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
UW Hindbrain Malformation Research Program, |
RCV000201682 | SCV000256390 | pathogenic | Joubert syndrome 5 | 2015-02-23 | criteria provided, single submitter | research | |
Labcorp Genetics |
RCV001383861 | SCV001583175 | pathogenic | Familial aplasia of the vermis; Meckel-Gruber syndrome; Nephronophthisis | 2023-12-02 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Leu1062Argfs*3) in the CEP290 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in CEP290 are known to be pathogenic (PMID: 16909394, 17345604, 20690115). This variant is not present in population databases (gnomAD no frequency). This premature translational stop signal has been observed in individuals with Joubert syndrome and/or Leber congenital amaurosis (PMID: 21153841, 26092869). ClinVar contains an entry for this variant (Variation ID: 217638). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus splice site. For these reasons, this variant has been classified as Pathogenic. |
Baylor Genetics | RCV003468925 | SCV004216564 | pathogenic | Bardet-Biedl syndrome 14 | 2024-02-20 | criteria provided, single submitter | clinical testing | |
Natera, |
RCV001835724 | SCV002094268 | pathogenic | Leber congenital amaurosis | 2020-03-12 | no assertion criteria provided | clinical testing |