Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001852664 | SCV002235006 | pathogenic | not provided | 2024-04-15 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg183*) in the OTOGL gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in OTOGL are known to be pathogenic (PMID: 23122586). This variant is present in population databases (rs397514588, gnomAD 0.007%). This premature translational stop signal has been observed in individual(s) with moderate hearing loss (PMID: 23122586). ClinVar contains an entry for this variant (Variation ID: 39779). 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 |
RCV001852664 | SCV005371424 | pathogenic | not provided | 2024-10-04 | 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: 24378291, 31980526, 23122586, 36360160) |
OMIM | RCV000033001 | SCV000056780 | pathogenic | Autosomal recessive nonsyndromic hearing loss 84B | 2012-11-02 | no assertion criteria provided | literature only | |
Prevention |
RCV003894841 | SCV004717158 | pathogenic | OTOGL-related disorder | 2023-10-18 | no assertion criteria provided | clinical testing | The OTOGL c.547C>T variant is predicted to result in premature protein termination (p.Arg183*). This variant was reported along with a splicing variant in three siblings with sensorineural hearing loss (Yariz. 2012. PubMed ID: 23122586; Oonk. 2014. PubMed ID: 24378291). This variant is reported in 0.0074% of alleles in individuals of European (Non-Finnish) descent in gnomAD (http://gnomad.broadinstitute.org/variant/12-80623121-C-T). Nonsense variants in OTOGL are expected to be pathogenic. This variant is interpreted as pathogenic. |