Total submissions: 11
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV000811923 | SCV000952214 | pathogenic | Neuronal ceroid lipofuscinosis | 2023-11-19 | 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 295 of the CLN3 protein (p.Glu295Lys). This variant is present in population databases (rs121434286, gnomAD 0.003%). This missense change has been observed in individual(s) with clinical features of inherited retinal dystrophy and neuronal ceroid lipofuscinosis (PMID: 9311735, 9450775, 24154662, 27486012). In at least one individual the data is consistent with being in trans (on the opposite chromosome) from a pathogenic variant. It has also been observed to segregate with disease in related individuals. ClinVar contains an entry for this variant (Variation ID: 3556). Advanced modeling of protein sequence and biophysical properties (such as structural, functional, and spatial information, amino acid conservation, physicochemical variation, residue mobility, and thermodynamic stability) performed at Invitae indicates that this missense variant is expected to disrupt CLN3 protein function with a positive predictive value of 80%. Experimental studies have shown that this missense change affects CLN3 function (PMID: 10332042, 16291725, 19132115). For these reasons, this variant has been classified as Pathogenic. |
Equipe Genetique des Anomalies du Developpement, |
RCV000055839 | SCV000965804 | pathogenic | Neuronal ceroid lipofuscinosis 3 | 2015-01-01 | criteria provided, single submitter | clinical testing | |
Institute of Human Genetics Munich, |
RCV000055839 | SCV001162797 | pathogenic | Neuronal ceroid lipofuscinosis 3 | 2019-06-11 | criteria provided, single submitter | clinical testing | |
Blueprint Genetics | RCV001074385 | SCV001239963 | pathogenic | Retinal dystrophy | 2019-08-06 | criteria provided, single submitter | clinical testing | |
Ambry Genetics | RCV002512720 | SCV003745354 | pathogenic | Inborn genetic diseases | 2020-11-04 | criteria provided, single submitter | clinical testing | The c.883G>A (p.E295K) alteration is located in exon 12 (coding exon 11) of the CLN3 gene. This alteration results from a G to A substitution at nucleotide position 883, causing the glutamic acid (E) at amino acid position 295 to be replaced by a lysine (K). Based on data from the Genome Aggregation Database (gnomAD) database, the CLN3 c.883G>A alteration was observed in 0.0025% (7/282860) of total alleles studied. This alteration has been detected in multiple affected individuals with a second disease-causing allele (Munroe, 1997; Wisniewski, 1998; Aberg, 2009) and has been reported to be associated with protracted disease when in trans with the common 1.02kb deletion in CLN3 (Cotman, 2012). This amino acid position is well conserved in available vertebrate species. The p.E295K alteration is predicted to be deleterious by in silico analysis. Based on the available evidence, this alteration is classified as pathogenic. |
Baylor Genetics | RCV000055839 | SCV004214324 | pathogenic | Neuronal ceroid lipofuscinosis 3 | 2024-03-07 | criteria provided, single submitter | clinical testing | |
Institute of Human Genetics, |
RCV001074385 | SCV005072672 | pathogenic | Retinal dystrophy | 2020-01-01 | criteria provided, single submitter | clinical testing | |
Mayo Clinic Laboratories, |
RCV004791194 | SCV005414345 | pathogenic | not provided | 2024-03-15 | criteria provided, single submitter | clinical testing | PP3, PP4, PM2_moderate, PM3_strong, PS3, PS4_moderate |
OMIM | RCV000003735 | SCV000023898 | pathogenic | Ceroid lipofuscinosis, neuronal, 3, protracted | 1998-01-01 | no assertion criteria provided | literature only | |
Gene |
RCV000055839 | SCV000086831 | pathologic | Neuronal ceroid lipofuscinosis 3 | 2013-08-01 | no assertion criteria provided | curation | Converted during submission to Pathogenic. |
Laboratory of Genetics in Ophthalmology, |
RCV001270479 | SCV001450771 | pathogenic | early onset and severe retinal dystrophy | no assertion criteria provided | research |