Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV001008272 | SCV001168038 | pathogenic | not provided | 2018-07-26 | criteria provided, single submitter | clinical testing | The c.6688_6689delAG variant in the ANKRD11 gene has not been reported previously as a pathogenic variant nor as a benign variant to our knowledge. The c.6688_6689delAG variant causes a frameshift starting with codon Arginine 2230, changes this amino acid to a Glycine residue, and creates a premature Stop codon at position 29 of the new reading frame, denoted p.Arg2230GlyfsX29. This variant is predicted to cause loss of normal protein function either through protein truncation or nonsense-mediated mRNA decay. The c.6688_6689delAG variant is not observed in large population cohorts (Lek et al., 2016). The presence of this pathogenic variant is consistent with the diagnosis of an ANKRD11-related disorder in this individual. |
Labcorp Genetics |
RCV005093048 | SCV005845780 | pathogenic | KBG syndrome | 2025-01-06 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg2230Glyfs*29) in the ANKRD11 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in ANKRD11 are known to be pathogenic (PMID: 21782149, 25125236, 25413698, 25652421). This variant is not present in population databases (gnomAD no frequency). This variant has not been reported in the literature in individuals affected with ANKRD11-related conditions. For these reasons, this variant has been classified as Pathogenic. |