Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Eurofins Ntd Llc |
RCV000337392 | SCV000342619 | likely pathogenic | not provided | 2016-06-06 | criteria provided, single submitter | clinical testing | |
Molecular Diagnostics Laboratory, |
RCV000760148 | SCV000889957 | pathogenic | Ullrich congenital muscular dystrophy 1A | 2017-06-29 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV002518040 | SCV003259904 | pathogenic | Bethlem myopathy 1A | 2022-01-21 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. Studies have shown that disruption of this splice site results in skipping of exon 18, but is expected to preserve the integrity of the reading-frame (PMID: 20976770). ClinVar contains an entry for this variant (Variation ID: 288503). Disruption of this splice site has been observed in individual(s) with clinical features of type VI/skeletal muscle collagenopathy (PMID: 20976770, 34167565). In at least one individual the variant was observed to be de novo. This variant is not present in population databases (gnomAD no frequency). This sequence change affects a donor splice site in intron 18 of the COL6A3 gene. It is expected to disrupt RNA splicing. Variants that disrupt the donor or acceptor splice site typically lead to a loss of protein function (PMID: 16199547), and loss-of-function variants in COL6A3 are known to be disease-causing for autosomal recessive COL6A3 conditions (PMID: 21280092, 20976770). However, certain variants affecting donor or acceptor splice sites in the triple helical domain of COL6A3 are expected to result in in-frame exon skipping and have been reported to cause autosomal dominant COL6A3-related conditions (PMID: 18366090). |