Total submissions: 5
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Eurofins Ntd Llc |
RCV000517732 | SCV000339086 | pathogenic | not provided | 2016-02-10 | criteria provided, single submitter | clinical testing | |
Athena Diagnostics | RCV000517732 | SCV000614802 | pathogenic | not provided | 2014-10-27 | criteria provided, single submitter | clinical testing | The variant results in a shift of the reading frame, and is therefore predicted to result in the loss of a functional protein. The frequency of this variant in the general population is consistent with pathogenicity. Found in multiple individuals with expected phenotype for this gene. |
Labcorp Genetics |
RCV001048951 | SCV001212981 | pathogenic | Charcot-Marie-Tooth disease type 4 | 2024-08-24 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Lys930Serfs*28) in the PRX gene. While this is not anticipated to result in nonsense mediated decay, it is expected to disrupt the last 532 amino acid(s) of the PRX protein. This variant is present in population databases (rs754521978, gnomAD 0.04%). This premature translational stop signal has been observed in individuals with Charcot-Marie-Tooth disease (PMID: 11133365). This variant is also known as S929fsX957. ClinVar contains an entry for this variant (Variation ID: 217239). This variant disrupts a region of the PRX protein in which other variant(s) (p.Arg1070*) have been determined to be pathogenic (PMID: 15197604, 15469949, 16770524, 22847150, 26059842). This suggests that this is a clinically significant region of the protein, and that variants that disrupt it are likely to be disease-causing. For these reasons, this variant has been classified as Pathogenic. |
Gene |
RCV000517732 | SCV003933479 | likely pathogenic | not provided | 2024-08-12 | criteria provided, single submitter | clinical testing | Frameshift variant predicted to result in abnormal protein length as the last 532 amino acids are replaced with 27 different amino acids, and other similar variants have been reported in HGMD; This variant is associated with the following publications: (PMID: 11133365) |
OMIM | RCV000005054 | SCV000025230 | pathogenic | Autosomal recessive Dejerine-Sottas syndrome | 2001-02-01 | no assertion criteria provided | literature only |