Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001938389 | SCV002195600 | pathogenic | not provided | 2021-06-10 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may create or strengthen a splice site, but this prediction has not been confirmed by published transcriptional studies. This variant has not been reported in the literature in individuals with COL4A1-related conditions. This variant is not present in population databases (ExAC no frequency). This sequence change creates a premature translational stop signal (p.Arg1063*) in the COL4A1 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in COL4A1 are known to be pathogenic (PMID: 23225343). |
Fulgent Genetics, |
RCV002484524 | SCV002794877 | likely pathogenic | Autosomal dominant familial hematuria-retinal arteriolar tortuosity-contractures syndrome; Brain small vessel disease 1 with or without ocular anomalies; Hemorrhage, intracerebral, susceptibility to; Retinal arterial tortuosity; Microangiopathy and leukoencephalopathy, pontine, autosomal dominant | 2022-03-11 | criteria provided, single submitter | clinical testing | |
Prevention |
RCV004529048 | SCV004112581 | likely pathogenic | COL4A1-related disorder | 2023-02-16 | criteria provided, single submitter | clinical testing | The COL4A1 c.3187C>T variant is predicted to result in premature protein termination (p.Arg1063*). To our knowledge, this variant has not been reported in the literature or in a large population database (http://gnomad.broadinstitute.org), indicating this variant is rare. Nonsense variants in COL4A1 are expected to be pathogenic. This variant is interpreted as likely pathogenic. |