Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Eurofins Ntd Llc |
RCV000374453 | SCV000337656 | likely pathogenic | not provided | 2015-11-10 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV000811810 | SCV000952097 | pathogenic | Mucopolysaccharidosis, MPS-II | 2018-08-17 | criteria provided, single submitter | clinical testing | This variant is not present in population databases (ExAC no frequency). This sequence change replaces cysteine with tyrosine at codon 422 of the IDS protein (p.Cys422Tyr). The cysteine residue is highly conserved and there is a large physicochemical difference between cysteine and tyrosine. This variant has been observed in individuals affected with mucopolysaccharidosis II (PMID: 26762690, 27246110, 24125893). ClinVar contains an entry for this variant (Variation ID: 284860). For these reasons, this variant has been classified as Pathogenic. Variants that disrupt the p.Cys422 amino acid residue in IDS have been observed in affected individuals (PMID: 26762690, 27246110, 24125893, 11683780, 1303211, 28077157). This suggests that it is a clinically significant residue, and that other variants that disrupt this residue are likely to be causative of disease. Algorithms developed to predict the effect of missense changes on protein structure and function are either unavailable or do not agree on the potential impact of this missense change (SIFT: "Deleterious"; PolyPhen-2: "Probably Damaging"; Align-GVGD: "Class C0"). |
Genome- |
RCV000811810 | SCV002014471 | likely pathogenic | Mucopolysaccharidosis, MPS-II | 2021-09-05 | criteria provided, single submitter | clinical testing | |
Laboratory of Diagnosis and Therapy of Lysosomal Disorders, |
RCV000811810 | SCV005089495 | pathogenic | Mucopolysaccharidosis, MPS-II | 2024-06-07 | criteria provided, single submitter | literature only | In vitro or in vivo functional studies supportive of a damaging effect (PS3_Moderate), Prevalence of the variant significantly increased in affected individuals compared with controls (PS4_Supporting), Located in a mutational hot spot and/or critical functional domain (PM1_Moderate), Absent from controls (or at low frequency) in gnomAD database (PM2_Moderate), Missense variant in a gene with a low rate of benign missense variation (PP2_Supporting), Multiple lines of computational evidence support a deleterious effect (PP3_Supporting), Patient’s phenotype or family history highly specific for the disease (PP4_Strong) |