Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Fulgent Genetics, |
RCV005005131 | SCV002813943 | likely pathogenic | Autosomal dominant Alport syndrome; Hematuria, benign familial, 2; Alport syndrome 3b, autosomal recessive | 2024-05-23 | criteria provided, single submitter | clinical testing | |
Prevention |
RCV003399042 | SCV004105825 | likely pathogenic | COL4A3-related disorder | 2023-03-22 | criteria provided, single submitter | clinical testing | The COL4A3 c.1468G>C variant is predicted to result in the amino acid substitution p.Gly490Arg. The p.Gly490 residue is located in the conserved triple helical domain, where substitutions of the glycine are usually pathogenic (UniProt residues 43-1438, Hudson et al. 1993. PubMed ID: 8253711; https://www.ncbi.nlm.nih.gov/books/NBK21582/). To our knowledge, this variant has not been reported in the literature, but has been reported in ClinVar as likely pathogenic by outside laboratories (https://www.ncbi.nlm.nih.gov/clinvar/variation/988108). This variant is reported in 0.00088% of alleles in individuals of European (Non-Finnish) descent in gnomAD (http://gnomad.broadinstitute.org/variant/2-228131768-G-C). This variant is interpreted as likely pathogenic. |
Sydney Genome Diagnostics, |
RCV001328060 | SCV001449248 | likely pathogenic | Alport syndrome | 2018-04-13 | no assertion criteria provided | clinical testing | This individual is heterozygous for the c.1468G>C variant in the COL4A3 gene. The variant has not been reported in any population databases (i.e. gnomAD, ExAC, ESP or dbSNP). To our knowledge, this variant has not been previously reported in the literature or any disease specific databases. This variant results in substitution of one of the invariant glycine residues within the triple helical domain of the alpha 3 chain of type 4 collagen. This variant is considered to be a likely pathogenic according to the ACMG guidelines. |