Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Genomic Medicine Center of Excellence, |
RCV000171462 | SCV000221661 | likely pathogenic | not provided | criteria provided, single submitter | research | ||
Labcorp Genetics |
RCV001852070 | SCV002238386 | pathogenic | Combined immunodeficiency with skin granulomas; Severe combined immunodeficiency, autosomal recessive, T cell-negative, B cell-negative, NK cell-positive | 2024-07-11 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.His468Argfs*16) in the RAG2 gene. While this is not anticipated to result in nonsense mediated decay, it is expected to disrupt the last 60 amino acid(s) of the RAG2 protein. This variant is not present in population databases (gnomAD no frequency). This premature translational stop signal has been observed in individual(s) with severe combined deficiency (PMID: 26915675). ClinVar contains an entry for this variant (Variation ID: 191271). This variant disrupts a region of the RAG2 protein in which other variant(s) (p.Glu480*) have been determined to be pathogenic (PMID: 21624848, 29772310). This suggests that this is a clinically significant region of the protein, and that variants that disrupt it are likely to be disease-causing. For these reasons, this variant has been classified as Pathogenic. |
Baylor Genetics | RCV003474922 | SCV004200550 | pathogenic | Combined immunodeficiency with skin granulomas | 2023-05-16 | criteria provided, single submitter | clinical testing |