Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001380993 | SCV001579236 | pathogenic | Mucolipidosis type II; Pseudo-Hurler polydystrophy | 2022-09-03 | criteria provided, single submitter | clinical testing | 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. ClinVar contains an entry for this variant (Variation ID: 1069206). Disruption of this splice site has been observed in individuals with mucolipidosis II and III (PMID: 16630736, 27662472). This variant is not present in population databases (gnomAD no frequency). This sequence change affects an acceptor splice site in intron 1 of the GNPTAB gene. It is expected to disrupt RNA splicing. Variants that disrupt the donor or acceptor splice site typically lead to a loss of protein function (PMID: 16199547), and loss-of-function variants in GNPTAB are known to be pathogenic (PMID: 19617216, 25107912). |
Fulgent Genetics, |
RCV001380993 | SCV005632601 | likely pathogenic | Mucolipidosis type II; Pseudo-Hurler polydystrophy | 2024-04-11 | criteria provided, single submitter | clinical testing | |
Department of Genetics and Endocrinology, |
RCV003984858 | SCV004041884 | pathogenic | Mucolipidosis | no assertion criteria provided | research |