Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001388840 | SCV001589990 | pathogenic | Telangiectasia, hereditary hemorrhagic, type 2 | 2020-02-17 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. Loss-of-function variants in ACVRL1 are known to be pathogenic (PMID: 15879500). This variant has not been reported in the literature in individuals with ACVRL1-related conditions. This variant is not present in population databases (ExAC no frequency). This sequence change creates a premature translational stop signal (p.Arg291*) in the ACVRL1 gene. It is expected to result in an absent or disrupted protein product. |
Ambry Genetics | RCV002377578 | SCV002685800 | pathogenic | Cardiovascular phenotype | 2021-12-07 | criteria provided, single submitter | clinical testing | The p.R291* pathogenic mutation (also known as c.871A>T), located in coding exon 6 of the ACVRL1 gene, results from an A to T substitution at nucleotide position 871. This changes the amino acid from an arginine to a stop codon within coding exon 6. This variant is considered to be rare based on population cohorts in the Genome Aggregation Database (gnomAD). In addition, this alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. As such, this alteration is interpreted as a disease-causing mutation. |