Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Ce |
RCV003333949 | SCV004042536 | pathogenic | not provided | 2023-09-01 | criteria provided, single submitter | clinical testing | AICDA: PVS1, PM2 |
Labcorp Genetics |
RCV000005434 | SCV004295835 | pathogenic | Hyper-IgM syndrome type 2 | 2024-01-22 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Cys147*) in the AICDA gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in AICDA are known to be pathogenic (PMID: 11007475). The frequency data for this variant in the population databases is considered unreliable, as metrics indicate poor data quality at this position in the gnomAD database. This premature translational stop signal has been observed in individual(s) with autosomal recessive hyper-IgM syndrome (PMID: 11007475). ClinVar contains an entry for this variant (Variation ID: 5127). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus splice site. For these reasons, this variant has been classified as Pathogenic. |
OMIM | RCV000005434 | SCV000025616 | pathogenic | Hyper-IgM syndrome type 2 | 2000-09-01 | no assertion criteria provided | literature only |