Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Institute of Human Genetics, |
RCV001262862 | SCV001440890 | likely pathogenic | Intellectual disability, autosomal recessive 42 | 2019-01-01 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001262862 | SCV002231956 | pathogenic | Intellectual disability, autosomal recessive 42 | 2024-10-17 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Leu681Argfs*4) in the PGAP1 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in PGAP1 are known to be pathogenic (PMID: 17711852, 26050939, 27848944). This variant is present in population databases (rs756609752, gnomAD 0.05%). This variant has not been reported in the literature in individuals affected with PGAP1-related conditions. ClinVar contains an entry for this variant (Variation ID: 983046). For these reasons, this variant has been classified as Pathogenic. |
Ambry Genetics | RCV002537640 | SCV003698269 | pathogenic | Inborn genetic diseases | 2022-05-09 | criteria provided, single submitter | clinical testing | The c.2042delT (p.L681Rfs*4) alteration, located in exon 22 (coding exon 22) of the PGAP1 gene, consists of a deletion of one nucleotide at position 2042, causing a translational frameshift with a predicted alternate stop codon after 4 amino acids. This alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. Based on the available evidence, this alteration is classified as pathogenic. |