Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000189694 | SCV000243341 | pathogenic | not provided | 2024-11-07 | 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 a significant frequency in large population cohorts (gnomAD); This variant is associated with the following publications: (PMID: 28292732, 28428906, 24387994, 28663785, 27541164, 24291220, 25169651, 26207815, 27281533, 25769375, 24469796, 29655203, 33929620, 31922275) |
Ambry Genetics | RCV000624622 | SCV000741956 | pathogenic | Inborn genetic diseases | 2017-01-09 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001217724 | SCV001389575 | pathogenic | Developmental and epileptic encephalopathy, 1; Autosomal dominant nonsyndromic hearing loss 65; Caused by mutation in the TBC1 domain family, member 24 | 2023-08-30 | 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: 207507). This premature translational stop signal has been observed in individual(s) with clinical features of autosomal recessive TBC1D24-related conditions (PMID: 31922275). In at least one individual the data is consistent with being in trans (on the opposite chromosome) from a pathogenic variant. This variant is present in population databases (rs765690011, gnomAD 0.002%). This sequence change creates a premature translational stop signal (p.Leu159Trpfs*10) 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). |