Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV000812139 | SCV000952443 | pathogenic | Primary ciliary dyskinesia | 2024-03-23 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg2795*) 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 (rs560398270, gnomAD 0.01%). This premature translational stop signal has been observed in individual(s) with clinical features of primary ciliary dyskinesia (PMID: 30067075). ClinVar contains an entry for this variant (Variation ID: 655872). For these reasons, this variant has been classified as Pathogenic. |
Ambry Genetics | RCV000812139 | SCV002680211 | pathogenic | Primary ciliary dyskinesia | 2019-01-26 | criteria provided, single submitter | clinical testing | The p.R2795* pathogenic mutation (also known as c.8383C>T), located in coding exon 50 of the DNAH5 gene, results from a C to T substitution at nucleotide position 8383. This changes the amino acid from an arginine to a stop codon within coding exon 50. 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. |
Natera, |
RCV000812139 | SCV002080847 | pathogenic | Primary ciliary dyskinesia | 2020-12-08 | no assertion criteria provided | clinical testing | |
Yale Center for Mendelian Genomics, |
RCV000812139 | SCV002106450 | likely pathogenic | Primary ciliary dyskinesia | 2018-08-01 | no assertion criteria provided | literature only |