Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Genomic Research Center, |
RCV000626131 | SCV000746761 | pathogenic | Methylmalonate semialdehyde dehydrogenase deficiency | 2020-05-03 | criteria provided, single submitter | clinical testing | |
Ambry Genetics | RCV002529778 | SCV003728291 | pathogenic | Inborn genetic diseases | 2021-01-27 | criteria provided, single submitter | clinical testing | The c.1156C>T (p.R386*) alteration, located in exon 9 (coding exon 9) of the ALDH6A1 gene, consists of a C to T substitution at nucleotide position 1156. This changes the amino acid from an arginine (R) to a stop codon at amino acid position 386. This alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. Based on data from the Genome Aggregation Database (gnomAD) database, the ALDH6A1 c.1156C>T alteration was observed in 0.01% (13/251344) of total alleles studied. Based on the available evidence, this alteration is classified as pathogenic. |
Labcorp Genetics |
RCV003767838 | SCV004654023 | uncertain significance | not provided | 2023-10-10 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg386*) in the ALDH6A1 gene. It is expected to result in an absent or disrupted protein product. However, the current clinical and genetic evidence is not sufficient to establish whether loss-of-function variants in ALDH6A1 cause disease. This variant is present in population databases (rs781767219, gnomAD 0.01%). This variant has not been reported in the literature in individuals affected with ALDH6A1-related conditions. ClinVar contains an entry for this variant (Variation ID: 522934). In summary, the available evidence is currently insufficient to determine the role of this variant in disease. Therefore, it has been classified as a Variant of Uncertain Significance. |