Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV000114348 | SCV001218442 | pathogenic | Aicardi-Goutieres syndrome 5 | 2023-09-21 | criteria provided, single submitter | clinical testing | This sequence change affects an acceptor splice site in intron 12 of the SAMHD1 gene. RNA analysis indicates that disruption of this splice site induces altered splicing and likely results in a shortened protein product. This variant is present in population databases (rs515726141, gnomAD 0.0009%). Disruption of this splice site has been observed in individual(s) with cerebral vasculopathy and early onset of stroke (PMID: 21402907). ClinVar contains an entry for this variant (Variation ID: 126407). Studies have shown that disruption of this splice site results in skipping of exon 13, but is expected to preserve the integrity of the reading-frame (PMID: 21402907). For these reasons, this variant has been classified as Pathogenic. |
Revvity Omics, |
RCV003137627 | SCV003827360 | pathogenic | not provided | 2022-05-16 | criteria provided, single submitter | clinical testing | |
Gene |
RCV003137627 | SCV005201557 | pathogenic | not provided | 2023-11-27 | criteria provided, single submitter | clinical testing | Canonical splice site variant predicted to result in an in-frame loss of the adjacent exon in a gene for which loss of function is a known mechanism of disease; Published functional studies demonstrate skipping of exon 13 and degradation of the SAMHD1 protein in cell lysates from an affected individual (PMID: 21402907); Not observed at significant frequency in large population cohorts (gnomAD); This variant is associated with the following publications: (PMID: 21633013, 31028937, 19525956, 28289923, 22461318, 34852373, 20301648, 21402907, 27943079) |
Gene |
RCV000114348 | SCV000147924 | not provided | Aicardi-Goutieres syndrome 5 | no assertion provided | literature only |