Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Institute for Human Genetics, |
RCV001376657 | SCV001478002 | likely pathogenic | Seizure | 2021-01-18 | criteria provided, single submitter | research | |
Pittsburgh Clinical Genomics Laboratory, |
RCV002246280 | SCV005397753 | likely pathogenic | Parenti-mignot neurodevelopmental syndrome | 2024-05-17 | criteria provided, single submitter | clinical testing | This sequence variant is a single nucleotide substitution (G>T) at position 940 of the coding sequence of the CHD5 gene that replaces Glu314 with an early termination codon. As it occurs in exon 7 of 42, this variant is predicted to generate a non-functional allele through either the expression of a truncated protein or a loss of CHD5-encoded chromodomain helicase DNA binding protein 5 expression due to nonsense-mediated decay. This is a previously reported variant (ClinVar 995777) that has been observed in a family with intellectual disability and/or craniosynostosis (PMID: 33944996). This variant is present in 2 of 1608952 alleles (0.00012%) in the gnomAD v4.1.0 population dataset. Haploinsufficiency in CHD5 is likely to be disease-causing (PMID: 33944996). Based upon the evidence, we consider this variant to be likely pathogenic. ACMG Criteria: PM2, PVS1 |
Gene |
RCV004822345 | SCV005443007 | pathogenic | not provided | 2024-07-01 | 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: 33944996) |
OMIM | RCV002246280 | SCV002520565 | pathogenic | Parenti-mignot neurodevelopmental syndrome | 2022-05-07 | no assertion criteria provided | literature only |