Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
UW Hindbrain Malformation Research Program, |
RCV000201612 | SCV000256375 | pathogenic | Joubert syndrome 5 | 2015-02-23 | criteria provided, single submitter | research | |
Labcorp Genetics |
RCV000686453 | SCV000813972 | pathogenic | Familial aplasia of the vermis; Meckel-Gruber syndrome; Nephronophthisis | 2023-01-25 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. ClinVar contains an entry for this variant (Variation ID: 217627). This premature translational stop signal has been observed in individual(s) with Joubert syndrome (PMID: 26092869). This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Val705Leufs*11) 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). |
Gene |
RCV002273985 | SCV002559632 | pathogenic | not provided | 2022-02-09 | criteria provided, single submitter | clinical testing | Frameshift variant predicted to result in protein truncation or nonsense mediated decay in a gene for which loss-of-function is a known mechanism of disease; Not observed at significant frequency in large population cohorts (gnomAD); This variant is associated with the following publications: (PMID: 26092869) |
Baylor Genetics | RCV003468920 | SCV004216696 | pathogenic | Bardet-Biedl syndrome 14 | 2023-02-26 | criteria provided, single submitter | clinical testing |