Total submissions: 6
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000002674 | SCV000793505 | pathogenic | Neuronal ceroid lipofuscinosis 5 | 2017-08-17 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV000689128 | SCV000816767 | pathogenic | Neuronal ceroid lipofuscinosis | 2023-12-27 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Trp75*) in the CLN5 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in CLN5 are known to be pathogenic (PMID: 20157158). This variant is present in population databases (rs104894385, gnomAD 0.006%). This premature translational stop signal has been observed in individual(s) with late infantile neuronal ceroid lipofuscinosis, and a CLN5-related condition (PMID: 9662406; Invitae). In at least one individual the data is consistent with being in trans (on the opposite chromosome) from a pathogenic variant. ClinVar contains an entry for this variant (Variation ID: 2565). For these reasons, this variant has been classified as Pathogenic. |
Genome- |
RCV000002674 | SCV001977472 | pathogenic | Neuronal ceroid lipofuscinosis 5 | 2021-08-10 | criteria provided, single submitter | clinical testing | |
OMIM | RCV000002674 | SCV000022832 | pathogenic | Neuronal ceroid lipofuscinosis 5 | 1998-07-01 | no assertion criteria provided | literature only | |
Gene |
RCV000002674 | SCV000086948 | not provided | Neuronal ceroid lipofuscinosis 5 | no assertion provided | literature only | ||
Natera, |
RCV000689128 | SCV002087941 | pathogenic | Neuronal ceroid lipofuscinosis | 2021-01-09 | no assertion criteria provided | clinical testing |