Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001210277 | SCV001381756 | pathogenic | not provided | 2023-08-28 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. ClinVar contains an entry for this variant (Variation ID: 940650). This premature translational stop signal has been observed in individual(s) with 11 beta-hydroxylase deficiency (PMID: 8506298, 12966519). This variant is present in population databases (no rsID available, gnomAD 0.006%). This sequence change creates a premature translational stop signal (p.Gln338*) in the CYP11B1 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in CYP11B1 are known to be pathogenic (PMID: 8506298, 26476331). |
Foundation for Research in Genetics and Endocrinology, |
RCV002291733 | SCV002583900 | pathogenic | Deficiency of steroid 11-beta-monooxygenase | 2022-01-10 | criteria provided, single submitter | clinical testing | A heterozygous missense variation in exon 6 of the ZMIZ1 gene that results in a stop codon and premature truncation of the protein at codon 409 (p.Gln409Ter) was detected.The c.1225C>T variant has not been reported in the 1000 genomes database and has not been reported in the gnomAD and genome databases. The reference codon is conserved across species. |
Fulgent Genetics, |
RCV005049788 | SCV005675079 | pathogenic | Deficiency of steroid 11-beta-monooxygenase; Glucocorticoid-remediable aldosteronism | 2024-01-12 | criteria provided, single submitter | clinical testing |