Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV000647369 | SCV000769164 | pathogenic | Glycogen storage disease IXc | 2017-11-12 | criteria provided, single submitter | clinical testing | Loss-of-function variants in PHKG2 are known to be pathogenic (PMID: 8896567, 17689125, 21646031). For these reasons, this variant has been classified as Pathogenic. This variant has not been reported in the literature in individuals with PHKG2-related disease. This sequence change creates a premature translational stop signal (p.Phe224*) in the PHKG2 gene. It is expected to result in an absent or disrupted protein product. This variant is not present in population databases (ExAC no frequency). |
Ambry Genetics | RCV003362877 | SCV004083859 | pathogenic | Inborn genetic diseases | 2023-07-25 | criteria provided, single submitter | clinical testing | The c.671_672delTCinsAA (p.F224*) alteration, located in exon 8 (coding exon 7) of the PHKG2 gene, consists of a deletion of 2 and insertion of 2 nucleotides at position 671 to 672. This changes the amino acid from a phenylalanine (F) to a stop codon at amino acid position 224. This alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. This variant was not reported in population-based cohorts in the Genome Aggregation Database (gnomAD). Based on the available evidence, this alteration is classified as pathogenic. |