Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001854929 | SCV002238761 | pathogenic | Citrin deficiency | 2023-10-19 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Gln259*) in the SLC25A13 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in SLC25A13 are known to be pathogenic (PMID: 10369257, 14680984, 27405544). This variant is not present in population databases (gnomAD no frequency). This premature translational stop signal has been observed in individuals with citrin deficiency (PMID: 21507300, 27405544). ClinVar contains an entry for this variant (Variation ID: 252920). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus splice site. For these reasons, this variant has been classified as Pathogenic. |
Baylor Genetics | RCV004567798 | SCV005056785 | pathogenic | Citrullinemia, type II, adult-onset | 2024-01-07 | criteria provided, single submitter | clinical testing | |
Fulgent Genetics, |
RCV005031829 | SCV005671936 | pathogenic | Neonatal intrahepatic cholestasis due to citrin deficiency; Citrullinemia, type II, adult-onset | 2024-04-03 | criteria provided, single submitter | clinical testing | |
Shenzhen Institute of Pediatrics, |
RCV000239387 | SCV000297735 | pathogenic | Neonatal intrahepatic cholestasis due to citrin deficiency | 2010-02-23 | no assertion criteria provided | clinical testing |