Total submissions: 9
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000404397 | SCV000329726 | pathogenic | not provided | 2022-06-07 | criteria provided, single submitter | clinical testing | 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; Not observed at significant frequency in large population cohorts (gnomAD); This variant is associated with the following publications: (PMID: 25525159, 16601880, 28714951, 27362913, 26179960, 31980526) |
Women's Health and Genetics/Laboratory Corporation of America, |
RCV000049445 | SCV000695755 | pathogenic | Glycine encephalopathy | 2016-10-14 | criteria provided, single submitter | clinical testing | Variant summary: The GLDC c.1009C>T (p.Arg337X) variant results in a premature termination codon, predicted to cause a truncated or absent GLDC protein due to nonsense mediated decay, which are commonly known mechanisms for disease. One in silico tool predicts a damaging outcome for this variant. This variant was found in 1/121360 control chromosomes at a frequency of 0.0000082, which does not exceed the estimated maximal expected allele frequency of a pathogenic GLDC variant (0.0026112). The variant has been reported in numerous affected individuals in the literature. In addition, one clinical diagnostic laboratory has classified this variant as likely pathogenic. Taken together, this variant is classified as pathogenic. |
Labcorp Genetics |
RCV000049445 | SCV000946606 | pathogenic | Glycine encephalopathy | 2024-01-04 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg337*) in the GLDC gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in GLDC are known to be pathogenic (PMID: 16601880). This variant is present in population databases (rs386833517, gnomAD 0.003%). This premature translational stop signal has been observed in individual(s) with glycine encephalopathy (PMID: 16601880, 26179960). ClinVar contains an entry for this variant (Variation ID: 56036). 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. |
Genomic Research Center, |
RCV000404397 | SCV001251720 | pathogenic | not provided | 2020-05-03 | criteria provided, single submitter | clinical testing | |
Laboratory of Medical Genetics, |
RCV004566898 | SCV005051798 | pathogenic | Glycine encephalopathy 1 | 2024-02-01 | criteria provided, single submitter | curation | |
Fulgent Genetics, |
RCV004566898 | SCV005679333 | pathogenic | Glycine encephalopathy 1 | 2024-03-21 | criteria provided, single submitter | clinical testing | |
Juha Muilu Group; Institute for Molecular Medicine Finland |
RCV000049445 | SCV000081879 | probable-pathogenic | Glycine encephalopathy | no assertion criteria provided | not provided | Converted during submission to Likely pathogenic. | |
Counsyl | RCV000049445 | SCV000790012 | pathogenic | Glycine encephalopathy | 2017-03-01 | no assertion criteria provided | clinical testing | |
Natera, |
RCV000049445 | SCV002075789 | pathogenic | Glycine encephalopathy | 2021-03-18 | no assertion criteria provided | clinical testing |