Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Genetic Services Laboratory, |
RCV001822118 | SCV002064385 | pathogenic | not provided | 2020-09-02 | criteria provided, single submitter | clinical testing | DNA sequence analysis of the SLC2A1 gene demonstrated a sequence change in exon 6, c.739G>T. This sequence change results in the creation of a premature stop codon at amino acid position 247, p.Glu247*. This sequence change is predicted to result in an abnormal transcript, which may be degraded, or may lead to the production of a truncated SLC2A1 (GLUT1) protein with potentially abnormal function. This sequence change is absent in the gnomAD population database. Other truncating variants in this region and downstream of this variant have been reported in glucose transporter type 1 deficiency syndrome (PMIDs: 20129935, 25487684, 10980529). Collectively these evidences indicate that, the p.Glu247* sequence change is pathogenic. |
Mendelics | RCV002246534 | SCV002519762 | pathogenic | Dystonia 9 | 2022-05-04 | criteria provided, single submitter | clinical testing | |
Genome- |
RCV003446921 | SCV004172966 | pathogenic | Encephalopathy due to GLUT1 deficiency | 2023-04-11 | criteria provided, single submitter | clinical testing |