Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Center of Genomic medicine, |
RCV000857220 | SCV000999804 | pathogenic | Infantile nephronophthisis | 2019-01-28 | criteria provided, single submitter | clinical testing | This variant was identified in composite heterozygosity with another variant in the same gene in a female patient with nephronophtisis, retinopathy and suspected ciliopathy |
Fulgent Genetics, |
RCV001535927 | SCV001752581 | likely pathogenic | Asphyxiating thoracic dystrophy 4; Nephronophthisis 12 | 2021-06-30 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001852034 | SCV002196147 | pathogenic | Jeune thoracic dystrophy; Nephronophthisis | 2023-08-07 | criteria provided, single submitter | clinical testing | ClinVar contains an entry for this variant (Variation ID: 30937). For these reasons, this variant has been classified as Pathogenic. Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus splice site. Disruption of this splice site has been observed in individual(s) with nephronophthisis (PMID: 21258341). In at least one individual the data is consistent with being in trans (on the opposite chromosome) from a pathogenic variant. This variant is present in population databases (rs766132877, gnomAD 0.005%). This sequence change affects an acceptor splice site in intron 20 of the TTC21B 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 TTC21B are known to be pathogenic (PMID: 18327258, 21068128, 21258341, 23559409, 24876116, 25492405, 27491411, 29068549). |
OMIM | RCV000023926 | SCV000045217 | pathogenic | Nephronophthisis 12 | 2011-03-01 | no assertion criteria provided | literature only |