Total submissions: 5
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV000525519 | SCV000636497 | uncertain significance | Bardet-Biedl syndrome | 2022-07-12 | criteria provided, single submitter | clinical testing | This sequence change replaces alanine, which is neutral and non-polar, with glycine, which is neutral and non-polar, at codon 349 of the TRIM32 protein (p.Ala349Gly). This variant is present in population databases (rs774316527, gnomAD 0.06%). This variant has not been reported in the literature in individuals affected with TRIM32-related conditions. ClinVar contains an entry for this variant (Variation ID: 462945). Algorithms developed to predict the effect of missense changes on protein structure and function output the following: SIFT: "Tolerated"; PolyPhen-2: "Benign"; Align-GVGD: "Class C0". The glycine amino acid residue is found in multiple mammalian species, which suggests that this missense change does not adversely affect protein function. 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. |
Eurofins Ntd Llc |
RCV000598259 | SCV000706133 | uncertain significance | not provided | 2017-02-21 | criteria provided, single submitter | clinical testing | |
Fulgent Genetics, |
RCV002476137 | SCV002801545 | uncertain significance | Sarcotubular myopathy; Bardet-Biedl syndrome 11 | 2022-04-06 | criteria provided, single submitter | clinical testing | |
Breakthrough Genomics, |
RCV000598259 | SCV005195549 | uncertain significance | not provided | criteria provided, single submitter | not provided | ||
Prevention |
RCV003935444 | SCV004755741 | uncertain significance | TRIM32-related disorder | 2023-12-31 | no assertion criteria provided | clinical testing | The TRIM32 c.1046C>G variant is predicted to result in the amino acid substitution p.Ala349Gly. To our knowledge, this variant has not been reported in the literature. This variant is reported in 0.062% of alleles in individuals of South Asian descent in gnomAD, which may be too frequent for a disease-causing variant. Although we suspect that this variant may be benign, at this time, the clinical significance of this variant is uncertain due to the absence of conclusive functional and genetic evidence. |