Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Women's Health and Genetics/Laboratory Corporation of America, |
RCV001192958 | SCV001361447 | pathogenic | Glucose-6-phosphate transport defect | 2019-10-11 | criteria provided, single submitter | clinical testing | Variant summary: SLC37A4 c.1179G>A (p.Trp393X) results in a premature termination codon, predicted to cause a truncation of the encoded protein or absence of the protein due to nonsense mediated decay, which are commonly known mechanisms for disease. The variant allele was found at a frequency of 1.6e-05 in 249216 control chromosomes (gnomAD). c.1179G>A has been reported in the literature in multiple individuals affected with Glycogen Storage Disease Type Ib (Choi_2017, Hiraiwa_1999, Prasad_2017, Santer_2000). These data indicate that the variant is very likely to be associated with disease. A functional study, Chen_2000, found the variant caused little to no SLC37A4 [referred to as G6PT (legacy name)] synthesis to occur. No clinical diagnostic laboratories have submitted clinical-significance assessments for this variant to ClinVar after 2014. Based on the evidence outlined above, the variant was classified as pathogenic. |
Labcorp Genetics |
RCV001192958 | SCV001592184 | pathogenic | Glucose-6-phosphate transport defect | 2023-04-18 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. This variant disrupts a region of the SLC37A4 protein in which other variant(s) (p.Arg415*) have been determined to be pathogenic (PMID: 10482962, 10931421, 15059622, 21575371). This suggests that this is a clinically significant region of the protein, and that variants that disrupt it are likely to be disease-causing. ClinVar contains an entry for this variant (Variation ID: 928687). This variant is also known as 1348G>A. This premature translational stop signal has been observed in individual(s) with clinical features of glycogen storage disease type Ib (PMID: 10923042, 29119402). This variant is present in population databases (no rsID available, gnomAD 0.006%). This sequence change creates a premature translational stop signal (p.Trp393*) in the SLC37A4 gene. While this is not anticipated to result in nonsense mediated decay, it is expected to disrupt the last 37 amino acid(s) of the SLC37A4 protein. |
Baylor Genetics | RCV001192958 | SCV004202453 | pathogenic | Glucose-6-phosphate transport defect | 2024-01-16 | criteria provided, single submitter | clinical testing | |
Natera, |
RCV001192958 | SCV002078563 | pathogenic | Glucose-6-phosphate transport defect | 2020-03-30 | no assertion criteria provided | clinical testing |