Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000669243 | SCV000793976 | pathogenic | Glycine encephalopathy | 2017-09-05 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV000669243 | SCV001580906 | pathogenic | Glycine encephalopathy | 2021-10-25 | criteria provided, single submitter | clinical testing | ClinVar contains an entry for this variant (Variation ID: 553731). This premature translational stop signal has been observed in individual(s) with glycine encephalopathy (PMID: 27362913). In at least one individual the data is consistent with the variant being in trans (on the opposite chromosome) from a pathogenic variant. This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Trp8*) in the GLDC gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in GLDC are known to be pathogenic (PMID: 16601880). For these reasons, this variant has been classified as Pathogenic. |
Prevention |
RCV003983163 | SCV004800470 | likely pathogenic | GLDC-related disorder | 2023-12-02 | no assertion criteria provided | clinical testing | The GLDC c.24G>A variant is predicted to result in premature protein termination (p.Trp8*). This variant was reported with a second GLDC variant in two individuals with non-ketotic hyperglycinemia (Coughlin et al. 2017. PubMed ID: 27362913). This variant has not been reported in a large population database, indicating this variant is rare. Nonsense variants in GLDC are expected to be pathogenic. This variant is interpreted as likely pathogenic. |