Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV002512791 | SCV003515305 | pathogenic | Epidermodysplasia verruciformis | 2023-12-22 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg94*) in the TMC6 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in TMC6 are known to be pathogenic (PMID: 15042430, 17139267). This variant is present in population databases (rs121908327, gnomAD 0.02%), including at least one homozygous and/or hemizygous individual. This premature translational stop signal has been observed in individual(s) with epidermodysplasia verruciformis (PMID: 12426567). It has also been observed to segregate with disease in related individuals. ClinVar contains an entry for this variant (Variation ID: 4748). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus splice site. For these reasons, this variant has been classified as Pathogenic. |
Gene |
RCV004719623 | SCV005325226 | pathogenic | not provided | 2023-11-22 | 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; This variant is associated with the following publications: (PMID: 25525159, 36705400, 18158319, 12426567) |
OMIM | RCV000005014 | SCV000025190 | risk factor | Epidermodysplasia verruciformis, susceptibility to, 1 | 2002-12-01 | no assertion criteria provided | literature only |