Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV003073544 | SCV003477261 | pathogenic | not provided | 2022-06-29 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg36*) in the IFT74 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in IFT74 are known to be pathogenic (PMID: 33531668). This variant is present in population databases (rs200556379, gnomAD 0.008%). This variant has not been reported in the literature in individuals affected with IFT74-related conditions. 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. |
Prevention |
RCV003434569 | SCV004117203 | likely pathogenic | IFT74-related disorder | 2024-04-26 | no assertion criteria provided | clinical testing | The IFT74 c.106C>T variant is predicted to result in premature protein termination (p.Arg36*). To our knowledge, this variant has not been reported in the literature. This variant is reported in 0.0078% of alleles in individuals of European (Non-Finnish) descent in gnomAD. Nonsense variants in IFT74 are expected to be pathogenic, including loss of function variants in exon 1 that are associated with Joubert syndrome (Luo et al. 2021. PubMed ID: 33531668). Taken together, this variant is interpreted as likely pathogenic. |