Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV001008129 | SCV001167888 | pathogenic | not provided | 2019-02-27 | criteria provided, single submitter | clinical testing | The c.2565_2568delGACT variant in the ADAR gene has been reported previously in an individual with Aicardi-Goutieres syndrome and an individual with bilateral striatal necrosis who were both heterozygous for the c.2565_2568delGACT variant and another ADAR variant (Rice et al., 2013; Livingston et al., 2014). In addition the c.2565_2568delGACT variant has been reported as a de novo variant in an individual with dyschromatosis symmetrica hereditaria (Li et al., 2014). The c.2565_2568delGACT variant causes a frameshift starting with codon Asparagine 857, changes this amino acid to an Alanine residue, and creates a premature Stop codon at position 17 of the new reading frame, denoted p.Asn857AlafsX17. This variant is predicted to cause loss of normal protein function either through protein truncation or nonsense-mediated mRNA decay. The c.2565_2568delGACT variant is not observed at a significant frequency in large population cohorts (Lek et al., 2016). We interpret c.2565_2568delGACT as a pathogenic variant. |
Suma Genomics | RCV001827169 | SCV002097008 | pathogenic | Aicardi-Goutieres syndrome 6 | criteria provided, single submitter | clinical testing | ||
Genome- |
RCV001827169 | SCV004050337 | pathogenic | Aicardi-Goutieres syndrome 6 | 2023-04-11 | criteria provided, single submitter | clinical testing |