Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Baylor Genetics | RCV000018579 | SCV001522654 | pathogenic | Complement component 5 deficiency | 2019-02-07 | criteria provided, single submitter | clinical testing | This variant was determined to be pathogenic according to ACMG Guidelines, 2015 [PMID:25741868]. |
Labcorp Genetics |
RCV001851917 | SCV002176466 | pathogenic | not provided | 2025-01-07 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg1476*) in the C5 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in C5 are known to be pathogenic (PMID: 7730648, 19414197, 27026170). This variant is present in population databases (rs121909588, gnomAD 0.05%). This premature translational stop signal has been observed in individual(s) with complement component 5 (C5) deficiency (PMID: 7730648). This variant is also known as p.Arg1458*. ClinVar contains an entry for this variant (Variation ID: 17051). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus splice site. For these reasons, this variant has been classified as Pathogenic. |
Fulgent Genetics, |
RCV002504806 | SCV002811049 | pathogenic | Complement component 5 deficiency; Eculizumab, poor response to | 2022-04-26 | criteria provided, single submitter | clinical testing | |
OMIM | RCV000018579 | SCV000038862 | pathogenic | Complement component 5 deficiency | 1995-05-15 | no assertion criteria provided | literature only |