Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001972569 | SCV002242694 | pathogenic | Familial aplasia of the vermis; Meckel-Gruber syndrome | 2022-04-16 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. 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.Tyr817*) 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, |
RCV005016953 | SCV005642053 | likely pathogenic | Joubert syndrome 7; Meckel syndrome, type 5; COACH syndrome 3 | 2024-06-04 | criteria provided, single submitter | clinical testing | |
Prevention |
RCV004728993 | SCV005337287 | likely pathogenic | RPGRIP1L-related disorder | 2024-08-15 | no assertion criteria provided | clinical testing | The RPGRIP1L c.2451C>A variant is predicted to result in premature protein termination (p.Tyr817*). To our knowledge, this variant has not been reported in the literature in individuals with RPGRIP1L-related disease, nor has this variant been reported in a large population database, indicating this variant is rare. Nonsense variants in RPGRIP1L are expected to be pathogenic. This variant is interpreted as likely pathogenic. |