Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001851500 | SCV002242039 | pathogenic | Developmental and epileptic encephalopathy, 1; Autosomal dominant nonsyndromic hearing loss 65; Caused by mutation in the TBC1 domain family, member 24 | 2022-02-04 | criteria provided, single submitter | clinical testing | This variant is present in population databases (rs267607103, gnomAD 0.0009%). For these reasons, this variant has been classified as Pathogenic. Experimental studies have shown that this missense change affects TBC1D24 function (PMID: 20727515). Advanced modeling of protein sequence and biophysical properties (such as structural, functional, and spatial information, amino acid conservation, physicochemical variation, residue mobility, and thermodynamic stability) performed at Invitae indicates that this missense variant is expected to disrupt TBC1D24 protein function. ClinVar contains an entry for this variant (Variation ID: 48). This missense change has been observed in individual(s) with autosomal recessive familial infantile myoclonic epilepsy (PMID: 20727515). It has also been observed to segregate with disease in related individuals. This sequence change replaces aspartic acid, which is acidic and polar, with histidine, which is basic and polar, at codon 147 of the TBC1D24 protein (p.Asp147His). |
OMIM | RCV000000065 | SCV000020208 | pathogenic | Familial infantile myoclonic epilepsy | 2010-09-10 | no assertion criteria provided | literature only | |
Division of Medical Genetics; Sainte- |
RCV000000065 | SCV000211971 | pathogenic | Familial infantile myoclonic epilepsy | 2014-12-22 | no assertion criteria provided | literature only |