Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Wendy Chung Laboratory, |
RCV002227158 | SCV002506552 | likely pathogenic | Episodic ataxia type 2; Spinocerebellar ataxia type 6; Migraine, familial hemiplegic, 1; Developmental and epileptic encephalopathy, 52 | 2022-03-20 | criteria provided, single submitter | clinical testing | |
Lupski Lab, |
RCV000416438 | SCV000494150 | pathogenic | Cerebellar ataxia | no assertion criteria provided | research | This variant was identified, de novo, in an individual with non-fluctuating ataxia. | |
Undiagnosed Diseases Network, |
RCV000556499 | SCV000622144 | likely pathogenic | Cerebellar ataxia; Intellectual disability; Cerebellar atrophy | 2015-12-19 | no assertion criteria provided | clinical testing | Likely pathogenicity based on finding it once in our study de novo in an 8-year-old female with delayed motor milestones, delayed speech, progressive cerebellar atrophy, hypotonia, and problems with coordination. Our patient has been reported in PMCID:PMC5557584 (patient 1). |
Prevention |
RCV004725207 | SCV005339107 | likely pathogenic | CACNA1A-related disorder | 2024-08-10 | no assertion criteria provided | clinical testing | The CACNA1A c.5015G>C variant is predicted to result in the amino acid substitution p.Arg1672Pro. This variant has been confirmed to be de novo in two unrelated individuals with CACNA1A-related disorders (Eldomery et al. 2017. PubMed ID: 28327206; Luo et al. 2017. PubMed ID: 28742085). In vivo modeling of this variant showed alternation in channel activation consistent with a gain-of-function effect (Luo et al. 2017. PubMed ID: 28742085; Tyagi et al. 2019. PubMed ID: 31015257). This variant has not been reported in a large population database, indicating this variant is rare and it is classified as likely pathogenic/pathogenic in ClinVar. Given the evidence, we interpret this variant as likely pathogenic. |