Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Ambry Genetics | RCV000621277 | SCV000740209 | pathogenic | Cardiovascular phenotype | 2017-08-14 | criteria provided, single submitter | clinical testing | The c.480delG pathogenic mutation, located in coding exon 4 of the MYBPC3 gene, results from a deletion of one nucleotide at nucleotide position 480, causing a translational frameshift with a predicted alternate stop codon (p.P161Hfs*6). 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. |
Gene |
RCV001008155 | SCV001167916 | pathogenic | not provided | 2023-12-26 | criteria provided, single submitter | clinical testing | Frameshift variant predicted to result in protein truncation or nonsense mediated decay in a gene for which loss of function is a known mechanism of disease; Not observed at significant frequency in large population cohorts (gnomAD); This variant is associated with the following publications: (PMID: 32344918) |
Labcorp Genetics |
RCV003767819 | SCV004642554 | pathogenic | Hypertrophic cardiomyopathy | 2023-03-01 | criteria provided, single submitter | clinical testing | This variant is not present in population databases (gnomAD no frequency). For these reasons, this variant has been classified as Pathogenic. ClinVar contains an entry for this variant (Variation ID: 520371). This variant is also known as p.P161Hfs*5. This premature translational stop signal has been observed in individual(s) with hypertrophic cardiomyopathy (PMID: 32344918). This sequence change creates a premature translational stop signal (p.Pro161Hisfs*6) in the MYBPC3 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in MYBPC3 are known to be pathogenic (PMID: 19574547). |