Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Fulgent Genetics, |
RCV001536012 | SCV001752692 | pathogenic | Asphyxiating thoracic dystrophy 4; Nephronophthisis 12 | 2021-06-30 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV003771653 | SCV004569694 | pathogenic | Jeune thoracic dystrophy; Nephronophthisis | 2023-12-29 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Glu90*) in the TTC21B gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in TTC21B are known to be pathogenic (PMID: 18327258, 21068128, 21258341, 23559409, 24876116, 25492405, 27491411, 29068549). This variant is present in population databases (rs748514860, gnomAD 0.08%). This premature translational stop signal has been observed in individual(s) with TTC21B-related conditions (PMID: 23559409, 25492405, 36263627). ClinVar contains an entry for this variant (Variation ID: 1179137). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may create or strengthen a splice site. For these reasons, this variant has been classified as Pathogenic. |
Department of Pediatrics, |
RCV003339667 | SCV004046853 | uncertain significance | Bardet-Biedl syndrome 2 | no assertion criteria provided | clinical testing |