Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001388801 | SCV001589941 | pathogenic | Familial aplasia of the vermis; Meckel-Gruber syndrome | 2022-12-31 | criteria provided, single submitter | clinical testing | Variants that disrupt the consensus splice site are a relatively common cause of aberrant splicing (PMID: 17576681, 9536098). Studies have shown that this variant results in skipping of exon 2 and introduces a premature termination codon (PMID: 27434533). The resulting mRNA is expected to undergo nonsense-mediated decay. ClinVar contains an entry for this variant (Variation ID: 1380). This variant has been observed in individual(s) with Joubert syndrome (PMID: 19058225, 27434533). In at least one individual the data is consistent with being in trans (on the opposite chromosome) from a pathogenic variant. This variant is not present in population databases (gnomAD no frequency). This sequence change falls in intron 2 of the TMEM67 gene. It does not directly change the encoded amino acid sequence of the TMEM67 protein. RNA analysis indicates that this variant induces altered splicing and may result in an absent or disrupted protein product. For these reasons, this variant has been classified as Pathogenic. |
Fulgent Genetics, |
RCV002496229 | SCV002808725 | pathogenic | COACH syndrome 1; Joubert syndrome 6; Meckel syndrome, type 3; RHYNS syndrome; Bardet-Biedl syndrome 14; Nephronophthisis 11 | 2022-03-24 | criteria provided, single submitter | clinical testing | |
OMIM | RCV000001448 | SCV000021598 | pathogenic | COACH syndrome 1 | 2009-02-01 | no assertion criteria provided | literature only |