Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000670997 | SCV000795931 | likely pathogenic | Autosomal recessive Alport syndrome | 2017-11-29 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001379464 | SCV001577267 | likely pathogenic | not provided | 2020-09-30 | criteria provided, single submitter | clinical testing | Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus splice site, but this prediction has not been confirmed by published transcriptional studies. This variant has been observed in individual(s) with clinical features of COL4A3-related conditions (invitae). ClinVar contains an entry for this variant (Variation ID: 555218). This variant is present in population databases (rs781566652, ExAC 0.01%). This sequence change affects a donor splice site in intron 42 of the COL4A3 gene. It is expected to disrupt RNA splicing and likely results in an absent or disrupted protein product. 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. Donor and acceptor splice site variants typically lead to a loss of protein function (PMID: 16199547), and loss-of-function variants in COL4A3 are known to be pathogenic (PMID: 8956999, 24854265, 26809805, 27281700). |
Natera, |
RCV001830450 | SCV002076422 | likely pathogenic | Alport syndrome | 2020-09-14 | no assertion criteria provided | clinical testing |