Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000410540 | SCV000486053 | likely pathogenic | Neuronal ceroid lipofuscinosis 3 | 2016-03-22 | criteria provided, single submitter | clinical testing | |
Mendelics | RCV000989587 | SCV001140077 | pathogenic | Neuronal ceroid lipofuscinosis | 2019-05-28 | criteria provided, single submitter | clinical testing | |
Baylor Genetics | RCV000410540 | SCV004214308 | likely pathogenic | Neuronal ceroid lipofuscinosis 3 | 2023-10-10 | criteria provided, single submitter | clinical testing | |
Invitae | RCV000989587 | SCV004426240 | pathogenic | Neuronal ceroid lipofuscinosis | 2023-01-07 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may create or strengthen a splice site. ClinVar contains an entry for this variant (Variation ID: 370675). This variant has not been reported in the literature in individuals affected with CLN3-related conditions. This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Cys353*) in the CLN3 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in CLN3 are known to be pathogenic (PMID: 9311735, 28542676). |