Total submissions: 5
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Clinical Genetics and Genomics, |
RCV001269528 | SCV001449574 | likely pathogenic | not provided | 2015-01-05 | criteria provided, single submitter | clinical testing | |
Institute of Medical Genetics and Applied Genomics, |
RCV001269528 | SCV001762125 | likely pathogenic | not provided | 2021-06-17 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001857880 | SCV002211490 | pathogenic | Jeune thoracic dystrophy | 2023-03-10 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. 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 DYNC2H1 protein function. ClinVar contains an entry for this variant (Variation ID: 446534). This missense change has been observed in individual(s) with clinical features of short-rib polydactyly syndrome (PMID: 29068549; Invitae). In at least one individual the data is consistent with being in trans (on the opposite chromosome) from a pathogenic variant. This variant is present in population databases (rs780600124, gnomAD 0.0009%). This sequence change replaces aspartic acid, which is acidic and polar, with asparagine, which is neutral and polar, at codon 3289 of the DYNC2H1 protein (p.Asp3289Asn). |
Dan Cohn Lab, |
RCV001291278 | SCV000611906 | pathogenic | Asphyxiating thoracic dystrophy 3 | 2017-06-01 | no assertion criteria provided | research | |
University of Washington Center for Mendelian Genomics, |
RCV001291278 | SCV001479719 | likely pathogenic | Asphyxiating thoracic dystrophy 3 | no assertion criteria provided | research |