Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000376321 | SCV000329614 | pathogenic | not provided | 2017-10-27 | criteria provided, single submitter | clinical testing | Although the c.395 G>A variant has not previously been reported to our knowledge, another nucleotide substitution, c.396 G>A, that also results in W132X has previously been reported in several unrelated individuals with primary carnitine deficiency (PCD) (Nezu et al., 1999;Tang et al., 1999; Ohkuma et al., 2009). The W132X nonsense variant in the SLC22A5 gene is predicted to cause loss of normal protein function either through protein truncation or nonsense-mediated mRNA decay. Therefore, we interpret W132X to be a pathogenic variant. |
Labcorp Genetics |
RCV001274463 | SCV003313084 | pathogenic | Renal carnitine transport defect | 2022-09-01 | 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 disrupt the consensus splice site. ClinVar contains an entry for this variant (Variation ID: 279949). This premature translational stop signal has been observed in individual(s) with clinical features of primary carnitine deficiency (PMID: 28841266, 32870709). This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Trp132*) in the SLC22A5 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in SLC22A5 are known to be pathogenic (PMID: 9916797). |
Natera, |
RCV001274463 | SCV001458685 | pathogenic | Renal carnitine transport defect | 2020-09-16 | no assertion criteria provided | clinical testing |