Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV001572114 | SCV001796698 | pathogenic | not provided | 2020-08-05 | criteria provided, single submitter | clinical testing | Canonical splice site variant predicted to result in a null allele in a gene for which loss-of-function is a known mechanism of disease; Not observed at a significant frequency in large population cohorts (Lek et al., 2016); This variant is associated with the following publications: (PMID: 23559409, 23188109) |
Labcorp Genetics |
RCV002546393 | SCV003522595 | likely pathogenic | Nephronophthisis | 2024-08-06 | criteria provided, single submitter | clinical testing | This sequence change affects a donor splice site in intron 18 of the NPHP3 gene. It is expected to disrupt RNA splicing. Variants that disrupt the donor or acceptor splice site typically lead to a loss of protein function (PMID: 16199547), and loss-of-function variants in NPHP3 are known to be pathogenic (PMID: 18371931, 23559409). This variant is present in population databases (no rsID available, gnomAD 0.004%). Disruption of this splice site has been observed in individual(s) with nephronophthisis (PMID: 23188109, 36090483). ClinVar contains an entry for this variant (Variation ID: 1029229). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus splice site. In summary, the currently available evidence indicates that the variant is pathogenic, but additional data are needed to prove that conclusively. Therefore, this variant has been classified as Likely Pathogenic. |
Fulgent Genetics, |
RCV005038085 | SCV005663574 | likely pathogenic | Renal-hepatic-pancreatic dysplasia 1; Nephronophthisis 3; NPHP3-related Meckel-like syndrome | 2024-03-15 | criteria provided, single submitter | clinical testing |