Total submissions: 5
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001215426 | SCV001387171 | pathogenic | Spastic paraplegia | 2023-08-03 | criteria provided, single submitter | clinical testing | ClinVar contains an entry for this variant (Variation ID: 944917). 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) has been performed at Invitae for this missense variant, however the output from this modeling did not meet the statistical confidence thresholds required to predict the impact of this variant on KIF5A protein function. This missense change has been observed in individuals with hereditary spastic paraplegia (PMID: 25352184, 27084214, 30778698). It has also been observed to segregate with disease in related individuals. This variant is present in population databases (rs748551786, gnomAD 0.003%). This sequence change replaces arginine, which is basic and polar, with tryptophan, which is neutral and slightly polar, at codon 162 of the KIF5A protein (p.Arg162Trp). |
Institute of Medical Genetics and Applied Genomics, |
RCV001268563 | SCV001447570 | pathogenic | not provided | 2020-10-23 | criteria provided, single submitter | clinical testing | |
Institute of Human Genetics, |
RCV003336339 | SCV004046789 | pathogenic | Hereditary spastic paraplegia 10 | criteria provided, single submitter | not provided | ||
Prevention |
RCV004548072 | SCV004113681 | likely pathogenic | KIF5A-related disorder | 2023-07-27 | criteria provided, single submitter | clinical testing | The KIF5A c.484C>T variant is predicted to result in the amino acid substitution p.Arg162Trp. This variant was reported in an individuals with hereditary spastic paraplegia and in at least one study segregate extensively with disease in a family (Supplementary Figure 2, Carosi et al 2015. PubMed ID: 25352184; Elert-Dobkowska et al. 2019. PubMed ID: 30778698). However in a different family, the variant was observed in unaffected individuals with different phenotypes than the initial report, indicating interfamilial phenotypic variability (Kaji et al. 2016. PubMed ID: 27084214). This variant is reported in 0.0033% of alleles in individuals of South Asian descent in gnomAD (http://gnomad.broadinstitute.org/variant/12-57958739-C-T). We interpret this variant as likely pathogenic. |
Gene |
RCV001268563 | SCV005324982 | likely pathogenic | not provided | 2023-11-15 | criteria provided, single submitter | clinical testing | Not observed at significant frequency in large population cohorts (gnomAD); In silico analysis supports that this missense variant has a deleterious effect on protein structure/function; This variant is associated with the following publications: (PMID: 27084214, 30778698, 33272564, 25352184) |