Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV002234794 | SCV000951088 | pathogenic | Familial focal epilepsy with variable foci | 2018-09-27 | criteria provided, single submitter | clinical testing | This variant has not been reported in the literature in individuals with DEPDC5-related disease. Loss-of-function variants in DEPDC5 are known to be pathogenic (PMID: 23542697, 23542701). For these reasons, this variant has been classified as Pathogenic. This sequence change creates a premature translational stop signal (p.Glu265Metfs*9) in the DEPDC5 gene. It is expected to result in an absent or disrupted protein product. This variant is not present in population databases (ExAC no frequency). |
Ambry Genetics | RCV002422784 | SCV002676993 | pathogenic | Inborn genetic diseases | 2018-12-26 | criteria provided, single submitter | clinical testing | The c.793_797delGAAGA pathogenic mutation, located in coding exon 12 of the DEPDC5 gene, results from a deletion of 5 nucleotides at nucleotide positions 793 to 797, causing a translational frameshift with a predicted alternate stop codon (p.E265Mfs*9). This alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. As such, this alteration is interpreted as a disease-causing mutation. |
Gene |
RCV004723226 | SCV005331912 | pathogenic | not provided | 2023-11-06 | criteria provided, single submitter | clinical testing | Frameshift 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: 23542697, 23542701, 31440721) |