Total submissions: 5
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Genome Diagnostics Laboratory, |
RCV001847631 | SCV002105664 | pathogenic | Hereditary spastic paraplegia | 2018-07-01 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV000034173 | SCV002236715 | pathogenic | Hereditary spastic paraplegia 11 | 2023-08-04 | criteria provided, single submitter | clinical testing | Studies have shown that disruption of this splice site results in skipping of exon 7 and introduces a premature termination codon (PMID: 18067136). The resulting mRNA is expected to undergo nonsense-mediated decay. ClinVar contains an entry for this variant (Variation ID: 41272). This variant is also known as c.1757-2A>G. Disruption of this splice site has been observed in individuals with hereditary spastic paraplegia (PMID: 18067136, 30778698). This variant is not present in population databases (gnomAD no frequency). This sequence change affects an acceptor splice site in intron 6 of the SPG11 gene. RNA analysis indicates that disruption of this splice site induces altered splicing and may result in an absent or disrupted protein product. For these reasons, this variant has been classified as Pathogenic. |
Genome- |
RCV000034173 | SCV002764133 | pathogenic | Hereditary spastic paraplegia 11 | criteria provided, single submitter | clinical testing | ||
Fulgent Genetics, |
RCV005007927 | SCV005637750 | likely pathogenic | Amyotrophic lateral sclerosis type 5; Hereditary spastic paraplegia 11; Charcot-Marie-Tooth disease axonal type 2X | 2024-03-23 | criteria provided, single submitter | clinical testing | |
Gene |
RCV000034173 | SCV000058111 | not provided | Hereditary spastic paraplegia 11 | no assertion provided | literature only |