Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV002243300 | SCV002512807 | likely pathogenic | not provided | 2022-04-19 | criteria provided, single submitter | clinical testing | Observed in probands with developmental delay (Faundes V et al., 2018); 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: 30217758, 28135719, 31785789, 29276005) |
Genomics England Pilot Project, |
RCV001542642 | SCV001760005 | likely pathogenic | Intellectual disability, autosomal recessive 65 | no assertion criteria provided | clinical testing | ||
Prevention |
RCV004728767 | SCV005340700 | likely pathogenic | KDM5B-related disorder | 2024-04-12 | no assertion criteria provided | clinical testing | The KDM5B c.2251C>T variant is predicted to result in premature protein termination (p.Arg751*). This variant has been repeatedly reported as de novo in individuals with intellectual disability and developmental delay phenotypes (Table S5, Faundes et al. 2018. PubMed ID: 29276005; Table S2, Turner et al. 2019. PubMed ID: 31785789). This variant is reported in 0.011% of alleles in individuals of African descent in gnomAD. Nonsense variants in KDM5B are expected to be pathogenic. This variant is interpreted as likely pathogenic. |