Total submissions: 10
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Genetic Services Laboratory, |
RCV000054513 | SCV000249104 | pathogenic | Intellectual disability, autosomal dominant 5 | 2015-01-05 | criteria provided, single submitter | clinical testing | |
Gene |
RCV000599367 | SCV000709920 | pathogenic | not provided | 2023-06-23 | 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: 23708187, 30541864, 31395010, 33144682, 31440721) |
Labcorp Genetics |
RCV000054513 | SCV000767491 | pathogenic | Intellectual disability, autosomal dominant 5 | 2023-11-27 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg143*) in the SYNGAP1 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in SYNGAP1 are known to be pathogenic (PMID: 23161826, 23708187, 26989088). This variant is not present in population databases (gnomAD no frequency). This premature translational stop signal has been observed in individual(s) with SYNGAP1-related conditions (PMID: 23708187, 30541864). In at least one individual the variant was observed to be de novo. ClinVar contains an entry for this variant (Variation ID: 60716). For these reasons, this variant has been classified as Pathogenic. |
Fulgent Genetics, |
RCV000054513 | SCV000893715 | pathogenic | Intellectual disability, autosomal dominant 5 | 2018-10-31 | criteria provided, single submitter | clinical testing | |
Ce |
RCV000599367 | SCV001248667 | pathogenic | not provided | 2023-02-01 | criteria provided, single submitter | clinical testing | SYNGAP1: PS2:Very Strong, PVS1, PM2, PS4:Moderate |
Génétique des Maladies du Développement, |
RCV000054513 | SCV001250625 | pathogenic | Intellectual disability, autosomal dominant 5 | criteria provided, single submitter | clinical testing | ||
Institute of Human Genetics, |
RCV000054513 | SCV002044440 | pathogenic | Intellectual disability, autosomal dominant 5 | 2021-12-10 | criteria provided, single submitter | clinical testing | This variant was identified as de novo (maternity and paternity confirmed)._x000D_ Criteria applied: PVS1, PS2, PS4_MOD, PM2_SUP |
Department of Clinical Genetics, |
RCV000054513 | SCV004801755 | pathogenic | Intellectual disability, autosomal dominant 5 | 2023-07-27 | criteria provided, single submitter | literature only | |
OMIM | RCV000054513 | SCV000082991 | pathogenic | Intellectual disability, autosomal dominant 5 | 2013-07-01 | no assertion criteria provided | literature only | |
Genome |
RCV001265523 | SCV001443667 | pathogenic | Complex neurodevelopmental disorder | 2018-04-16 | no assertion criteria provided | provider interpretation | Submission from Simons Searchlight facilitated by GenomeConnect. Variant interpreted by the Simons Searchlight team most recently on 2018-04-16 and interpreted as Pathogenic. Variant was initially reported on 2017-10-09 by GTR ID of laboratory name 500031. The reporting laboratory might also submit to ClinVar. |