Total submissions: 5
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000674101 | SCV000799377 | likely pathogenic | Primary ciliary dyskinesia 3 | 2018-04-16 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV000689854 | SCV000817523 | pathogenic | Primary ciliary dyskinesia | 2022-10-14 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Trp4206*) in the DNAH5 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in DNAH5 are known to be pathogenic (PMID: 11788826, 16627867). This variant is present in population databases (rs372118787, gnomAD 0.007%). This variant has not been reported in the literature in individuals affected with DNAH5-related conditions. ClinVar contains an entry for this variant (Variation ID: 557901). For these reasons, this variant has been classified as Pathogenic. |
Hudson |
RCV000674101 | SCV001439379 | pathogenic | Primary ciliary dyskinesia 3 | 2020-09-18 | criteria provided, single submitter | research | ACMG codes:PVS1, PM2, PM3, PP5 |
Ambry Genetics | RCV000689854 | SCV002680247 | pathogenic | Primary ciliary dyskinesia | 2018-05-17 | criteria provided, single submitter | clinical testing | The p.W4206* pathogenic mutation (also known as c.12617G>A), located in coding exon 73 of the DNAH5 gene, results from a G to A substitution at nucleotide position 12617. This changes the amino acid from a tryptophan to a stop codon within coding exon 73. 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. |
Yale Center for Mendelian Genomics, |
RCV000689854 | SCV002106454 | likely pathogenic | Primary ciliary dyskinesia | 2018-08-01 | no assertion criteria provided | literature only |