Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000436259 | SCV000534816 | pathogenic | not provided | 2024-07-10 | criteria provided, single submitter | clinical testing | Observed multiple times with a pathogenic variant on the opposite allele (in trans) in unrelated patients with drug-resistant epilepsy and developmental delay (PMID: 27502353); 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: 32549035, 27502353, 31440721) |
Labcorp Genetics |
RCV000697787 | SCV000826417 | pathogenic | Developmental and epileptic encephalopathy, 1; Autosomal dominant nonsyndromic hearing loss 65; Caused by mutation in the TBC1 domain family, member 24 | 2022-02-10 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. ClinVar contains an entry for this variant (Variation ID: 391687). This premature translational stop signal has been observed in individual(s) with autosomal recessive TBC1D24-related epilepsy (PMID: 27502353). This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Gln41*) in the TBC1D24 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in TBC1D24 are known to be pathogenic (PMID: 23526554, 24291220). |