Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
IIFP, |
RCV000204452 | SCV000262536 | pathogenic | Mucopolysaccharidosis, MPS-II | 2011-12-05 | criteria provided, single submitter | research | |
Labcorp Genetics |
RCV000204452 | SCV004299010 | pathogenic | Mucopolysaccharidosis, MPS-II | 2023-06-13 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. Variants that disrupt the consensus splice site are a relatively common cause of aberrant splicing (PMID: 17576681, 9536098). Studies have shown that disruption of this splice site results in activation of a cryptic splice site and introduces a new termination codon (PMID: 7728156, 27883178). However the mRNA is not expected to undergo nonsense-mediated decay. ClinVar contains an entry for this variant (Variation ID: 221218). Disruption of this splice site has been observed in individual(s) with mucopolysaccharidosis type II (PMID: 7728156, 17063374, 27883178, 34813777, 35144014). This variant is not present in population databases (gnomAD no frequency). This sequence change affects an acceptor splice site in intron 8 of the IDS gene. RNA analysis indicates that disruption of this splice site induces altered splicing and likely disrupts the C-terminus of the protein. |
Laboratory of Diagnosis and Therapy of Lysosomal Disorders, |
RCV000204452 | SCV005089460 | likely pathogenic | Mucopolysaccharidosis, MPS-II | 2024-06-07 | criteria provided, single submitter | literature only | Null variant (PVS1_Strong), Prevalence of the variant significantly increased in affected individuals compared with controls (PS4_Supporting), Absent from controls (or at low frequency) in gnomAD database (PM2_Moderate), Patient’s phenotype or family history highly specific for the disease (PP4_Moderate) |
Pediatrics, |
RCV000204452 | SCV001573801 | affects | Mucopolysaccharidosis, MPS-II | 2014-04-12 | no assertion criteria provided | research | The change c.1181-1G>A is a known splice donor variant. This mutation is due to substitution of G to A at nucleotide position c.1181-1G>A in the intron 8 of IDS gene. It was detected in a hemizygous state in one patient with attenuated phenotype from Delhi, India. |