Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001235875 | SCV001408581 | pathogenic | Familial hypercholesterolemia | 2021-07-28 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. Loss-of-function variants in LDLR are known to be pathogenic (PMID: 20809525, 28645073). This variant has not been reported in the literature in individuals with LDLR-related conditions. ClinVar contains an entry for this variant (Variation ID: 440565). This variant is not present in population databases (ExAC no frequency). This sequence change creates a premature translational stop signal (p.Phe126Leufs*80) in the LDLR gene. It is expected to result in an absent or disrupted protein product. |
Ambry Genetics | RCV002367700 | SCV002625810 | pathogenic | Cardiovascular phenotype | 2020-07-24 | criteria provided, single submitter | clinical testing | The c.378delC variant, located in coding exon 4 of the LDLR gene, results from a deletion of one nucleotide at nucleotide position 378, causing a translational frameshift with a predicted alternate stop codon (p.F126Lfs*80). 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. |
Laboratorium voor Moleculaire Diagnostiek Experimentele Vasculaire Geneeskunde, |
RCV000508704 | SCV000606100 | pathogenic | Hypercholesterolemia, familial, 1 | no assertion criteria provided | research |