Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001045131 | SCV001208965 | pathogenic | Deficiency of acetyl-CoA acetyltransferase | 2024-01-28 | criteria provided, single submitter | clinical testing | This variant results in the deletion of part of exon 1 (c.64_72+10del) of the ACAT1 gene. It is expected to disrupt RNA splicing. Variants that disrupt the donor or acceptor splice site typically lead to a loss of protein function (PMID: 16199547), and loss-of-function variants in ACAT1 are known to be pathogenic (PMID: 7749408). This variant is present in population databases (no rsID available, gnomAD 0.03%). This variant has been observed in individual(s) with beta-ketothiolase deficiency (Invitae). In at least one individual the data is consistent with being in trans (on the opposite chromosome) from a pathogenic variant. ClinVar contains an entry for this variant (Variation ID: 842676). For these reasons, this variant has been classified as Pathogenic. |
Baylor Genetics | RCV001045131 | SCV004210464 | likely pathogenic | Deficiency of acetyl-CoA acetyltransferase | 2024-03-04 | criteria provided, single submitter | clinical testing | |
Fulgent Genetics, |
RCV001045131 | SCV005680510 | likely pathogenic | Deficiency of acetyl-CoA acetyltransferase | 2024-03-29 | criteria provided, single submitter | clinical testing | |
Natera, |
RCV001045131 | SCV002094716 | likely pathogenic | Deficiency of acetyl-CoA acetyltransferase | 2020-09-02 | no assertion criteria provided | clinical testing |