Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000144786 | SCV000191010 | pathogenic | not provided | 2014-03-28 | criteria provided, single submitter | clinical testing | The c.1671_1672insA (aka c.1671dupA) mutation in the CDKL5 gene has been reported previously in association with CDKL5-related disorders (Fehr et al., 2013). The duplication causes a frameshift starting with codon Arginine 558, changes this amino acid to a Threonine residue and creates a premature Stop codon at position 9 of the new reading frame, denoted p.Arg558ThrfsX9. This mutation is predicted to cause loss of normal protein function either through protein truncation or nonsense-mediated mRNA decay. The variant is found in INFANT-EPI panel(s). |
Revvity Omics, |
RCV003137646 | SCV003823104 | likely pathogenic | Developmental and epileptic encephalopathy, 2 | 2022-11-04 | criteria provided, single submitter | clinical testing | |
Centre for Population Genomics, |
RCV004724918 | SCV005335239 | pathogenic | CDKL5 disorder | 2024-09-20 | criteria provided, single submitter | curation | This variant has been collected from RettBASE and curated to current modified ACMG/AMP criteria. Based on the classification scheme defined by the ClinGen Rett/Angelman-like Expert Panel for Rett/AS-like Disorders Specifications to the ACMG/AMP Variant Interpretation Guidelines VCEP 3.0, this variant is classified as pathogenic. At least the following criteria are met: Predicted to result in loss of function, and LOF is a known mechanism of disease (PVS1). This variant is absent from gnomAD v4 (PM2_Supporting). Has been observed in at least 2 individuals with phenotypes consistent with CDKL5 disorder (PS4_Supporting). PMID:25657822, Variation ID: 156643 |