Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001231979 | SCV001404518 | pathogenic | Familial aplasia of the vermis; Meckel-Gruber syndrome | 2023-04-26 | criteria provided, single submitter | clinical testing | 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 create or strengthen a splice site. ClinVar contains an entry for this variant (Variation ID: 958759). This variant has not been reported in the literature in individuals affected with RPGRIP1L-related conditions. This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Lys1041*) in the RPGRIP1L gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in RPGRIP1L are known to be pathogenic (PMID: 17558409). |
Fulgent Genetics, |
RCV002497792 | SCV002813944 | likely pathogenic | Joubert syndrome 7; Meckel syndrome, type 5; COACH syndrome 3 | 2022-04-01 | criteria provided, single submitter | clinical testing | |
Prevention |
RCV004538486 | SCV004116169 | likely pathogenic | RPGRIP1L-related disorder | 2023-12-04 | no assertion criteria provided | clinical testing | The RPGRIP1L c.3121A>T variant is predicted to result in premature protein termination (p.Lys1041*). To our knowledge, this variant has not been reported in the literature. This variant is reported in 0.00088% of alleles in individuals of European (Non-Finnish) descent in gnomAD. Nonsense variants in RPGRIP1L are expected to be pathogenic. This variant is interpreted as likely pathogenic. |