Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001856217 | SCV002186569 | uncertain significance | not provided | 2022-08-16 | criteria provided, single submitter | clinical testing | This sequence change replaces glutamic acid, which is acidic and polar, with lysine, which is basic and polar, at codon 1250 of the PTPN23 protein (p.Glu1250Lys). This variant is present in population databases (rs148689441, gnomAD 0.01%). This missense change has been observed in individual(s) with clinical features of PTPN23-related conditions (PMID: 31395947). ClinVar contains an entry for this variant (Variation ID: 636315). 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 tolerated. 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. |
Ambry Genetics | RCV004027360 | SCV004935254 | uncertain significance | Inborn genetic diseases | 2024-03-14 | criteria provided, single submitter | clinical testing | The c.3748G>A (p.E1250K) alteration is located in exon 20 (coding exon 20) of the PTPN23 gene. This alteration results from a G to A substitution at nucleotide position 3748, causing the glutamic acid (E) at amino acid position 1250 to be replaced by a lysine (K). Based on insufficient or conflicting evidence, the clinical significance of this alteration remains unclear. |
Regeneron Genetics Center, |
RCV000853202 | SCV000927109 | likely pathogenic | Global developmental delay; Brain atrophy | 2019-02-15 | no assertion criteria provided | research | Identified in cohort of patients with neurodevelopmental disorder accompanied by structural brain abnormalities |