Total submissions: 5
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
3billion | RCV002283458 | SCV002572683 | pathogenic | Ketoacidosis due to monocarboxylate transporter-1 deficiency | 2022-09-01 | criteria provided, single submitter | clinical testing | The variant is observed at an extremely low frequency in the gnomAD v2.1.1 dataset (total allele frequency: <0.001%). Stop-gained (nonsense) is predicted to result in a loss or disruption of normal protein function through nonsense-mediated decay (NMD) or protein truncation. Multiple pathogenic variants are reported downstream of the variant. Functional studies provide strong evidence of the variant having a damaging effect on the gene or gene product (PMID: 25390740). The variant has been reported to be associated with SLC16A1-related disorder (ClinVar ID: VCV000158079 / PMID: 25390740). Therefore, this variant is classified as Pathogenic according to the recommendation of ACMG/AMP guideline. |
Pediatric/Medical Genetics, |
RCV002283458 | SCV002765160 | pathogenic | Ketoacidosis due to monocarboxylate transporter-1 deficiency | criteria provided, single submitter | clinical testing | ||
Labcorp Genetics |
RCV003556185 | SCV004291970 | pathogenic | not provided | 2023-12-18 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg313*) in the SLC16A1 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in SLC16A1 are known to be pathogenic (PMID: 25390740). This variant is present in population databases (rs606231299, gnomAD 0.006%). This premature translational stop signal has been observed in individual(s) with autosomal recessive SLC16A1-related conditions (PMID: 25390740). ClinVar contains an entry for this variant (Variation ID: 158079). For these reasons, this variant has been classified as Pathogenic. |
Gene |
RCV003556185 | SCV005325218 | pathogenic | not provided | 2023-12-13 | criteria provided, single submitter | clinical testing | Not observed at significant frequency in large population cohorts (gnomAD); Nonsense variant predicted to result in protein truncation or nonsense mediated decay in a gene for which loss of function is a known mechanism of disease; This variant is associated with the following publications: (PMID: 35729663, 25390740) |
OMIM | RCV000145408 | SCV000192497 | pathogenic | Monocarboxylate transporter 1 deficiency, autosomal recessive | 2014-11-13 | no assertion criteria provided | literature only |