Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV000803615 | SCV000943495 | uncertain significance | Cutis laxa, autosomal recessive, type 1B | 2022-06-27 | criteria provided, single submitter | clinical testing | This sequence change replaces glutamic acid, which is acidic and polar, with lysine, which is basic and polar, at codon 94 of the EFEMP2 protein (p.Glu94Lys). This variant is present in population databases (rs370848091, gnomAD 0.01%). This variant has not been reported in the literature in individuals affected with EFEMP2-related conditions. ClinVar contains an entry for this variant (Variation ID: 648809). Algorithms developed to predict the effect of missense changes on protein structure and function are either unavailable or do not agree on the potential impact of this missense change (SIFT: "Deleterious"; PolyPhen-2: "Benign"; Align-GVGD: "Class C0"). In summary, the available evidence is currently insufficient to determine the role of this variant in disease. Therefore, it has been classified as a Variant of Uncertain Significance. |
Ambry Genetics | RCV002440696 | SCV002749239 | uncertain significance | Cardiovascular phenotype | 2022-09-19 | criteria provided, single submitter | clinical testing | The p.E94K variant (also known as c.280G>A), located in coding exon 3 of the EFEMP2 gene, results from a G to A substitution at nucleotide position 280. The glutamic acid at codon 94 is replaced by lysine, an amino acid with similar properties. This amino acid position is well conserved in available vertebrate species. In addition, the in silico prediction for this alteration is inconclusive. Since supporting evidence is limited at this time, the clinical significance of this alteration remains unclear. |
Gene |
RCV002473144 | SCV002770359 | uncertain significance | not provided | 2024-07-24 | criteria provided, single submitter | clinical testing | Not observed at significant frequency in large population cohorts (gnomAD); In silico analysis indicates that this missense variant does not alter protein structure/function; Has not been previously published as pathogenic or benign to our knowledge |