Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Prevention |
RCV003394139 | SCV004121287 | pathogenic | ENAM-related disorder | 2022-11-07 | criteria provided, single submitter | clinical testing | The ENAM c.588+1delG variant is predicted to result in a deletion affecting a canonical splice site. This is one of the most frequently reported variants in individuals with autosomal dominant hypoplastic amelogenesis imperfecta (Wright et al. 2011. PubMed ID: 21597265; Zhang et al. 2019. PubMed ID: 31478359). This variant has not been reported in a large population database (http://gnomad.broadinstitute.org), indicating this variant is rare. This variant is interpreted as pathogenic. |
Gene |
RCV004591549 | SCV005078566 | pathogenic | not provided | 2024-07-11 | criteria provided, single submitter | clinical testing | Published functional studies demonstrate a damaging effect as the truncated protein was refractory to secretion and increased the ER stress response and apoptosis, and decreased cell survival (PMID: 38716742); Not observed in large population cohorts (gnomAD); This variant is associated with the following publications: (PMID: 31478359, 21597265, 12828988, 38716742, 12407086) |
Wang Lab, |
RCV001554271 | SCV001775496 | pathogenic | Amelogenesis imperfecta - hypoplastic autosomal dominant - local | 2021-08-09 | no assertion criteria provided | research |