Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Institute of Medical Genetics and Applied Genomics, |
RCV001543536 | SCV001762161 | pathogenic | not provided | 2021-06-17 | criteria provided, single submitter | clinical testing | |
Ambry Genetics | RCV004651687 | SCV005138961 | pathogenic | Inborn genetic diseases | 2024-04-26 | criteria provided, single submitter | clinical testing | The c.1149delC (p.A384Lfs*29) alteration, located in exon 11 (coding exon 10) of the NPRL3 gene, consists of a deletion of one nucleotide at position 1149, causing a translational frameshift with a predicted alternate stop codon after 29 amino acids. 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. |
Labcorp Genetics |
RCV005094762 | SCV005759478 | pathogenic | Epilepsy, familial focal, with variable foci 3 | 2024-06-20 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Ala384Leufs*29) in the NPRL3 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in NPRL3 are known to be pathogenic (PMID: 26285051, 26505888). This variant is not present in population databases (gnomAD no frequency). This variant has not been reported in the literature in individuals affected with NPRL3-related conditions. ClinVar contains an entry for this variant (Variation ID: 1184941). For these reasons, this variant has been classified as Pathogenic. |