Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV000703436 | SCV000832335 | uncertain significance | Multiple congenital anomalies-hypotonia-seizures syndrome 1 | 2022-08-09 | criteria provided, single submitter | clinical testing | This sequence change replaces aspartic acid, which is acidic and polar, with glycine, which is neutral and non-polar, at codon 57 of the PIGN protein (p.Asp57Gly). This variant is present in population databases (rs745318716, gnomAD 0.05%). This variant has not been reported in the literature in individuals affected with PIGN-related conditions. ClinVar contains an entry for this variant (Variation ID: 580016). Algorithms developed to predict the effect of missense changes on protein structure and function (SIFT, PolyPhen-2, Align-GVGD) all suggest that this variant is likely to be disruptive. Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may create or strengthen a splice site. 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. |
Institute of Human Genetics, |
RCV000703436 | SCV001429509 | uncertain significance | Multiple congenital anomalies-hypotonia-seizures syndrome 1 | 2017-12-05 | criteria provided, single submitter | clinical testing | This variant was identified as homozygous |
Revvity Omics, |
RCV000703436 | SCV003808348 | uncertain significance | Multiple congenital anomalies-hypotonia-seizures syndrome 1 | 2021-03-02 | criteria provided, single submitter | clinical testing | |
Ambry Genetics | RCV003362913 | SCV004056124 | uncertain significance | Inborn genetic diseases | 2023-08-19 | criteria provided, single submitter | clinical testing | The c.170A>G (p.D57G) alteration is located in exon 4 (coding exon 1) of the PIGN gene. This alteration results from a A to G substitution at nucleotide position 170, causing the aspartic acid (D) at amino acid position 57 to be replaced by a glycine (G). Based on insufficient or conflicting evidence, the clinical significance of this alteration remains unclear. |