Total submissions: 4
| Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
|---|---|---|---|---|---|---|---|---|
| Gene |
RCV000356915 | SCV000330020 | pathogenic | not provided | 2024-09-19 | criteria provided, single submitter | clinical testing | Frameshift variant predicted to result in protein truncation or nonsense mediated decay in a gene for which loss of function is a known mechanism of disease; This variant is associated with the following publications: (PMID: 15554930, 31589614) |
| Labcorp Genetics |
RCV000356915 | SCV002225017 | pathogenic | not provided | 2024-04-29 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.His643Profs*10) in the C7 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in C7 are known to be pathogenic (PMID: 9856499, 17407100). This variant is present in population databases (rs764871530, gnomAD 0.06%). This premature translational stop signal has been observed in individual(s) with C7 deficiency: (PMID: 15554930). This variant is also known as 1924delAG; S620 X 630. ClinVar contains an entry for this variant (Variation ID: 280140). For these reasons, this variant has been classified as Pathogenic. |
| Fulgent Genetics, |
RCV002259331 | SCV002807803 | pathogenic | Complement component 7 deficiency | 2021-12-04 | criteria provided, single submitter | clinical testing | |
| OMIM | RCV002259331 | SCV000033134 | pathogenic | Complement component 7 deficiency | 2006-06-01 | no assertion criteria provided | literature only |