Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Laboratory of Medical Genetics, |
RCV000239652 | SCV001976905 | uncertain significance | Encephalopathy, lethal, due to defective mitochondrial peroxisomal fission 1 | 2021-10-06 | criteria provided, single submitter | clinical testing | PVS1, PM2 |
Labcorp Genetics |
RCV001854933 | SCV002124972 | pathogenic | not provided | 2023-12-02 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Glu116Lysfs*6) in the DNM1L gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in DNM1L are known to be pathogenic (PMID: 26825290, 27328748). This variant is present in population databases (rs779230636, gnomAD 0.009%). This premature translational stop signal has been observed in individuals with autosomal recessive encephalopathy (PMID: 26825290, 27328748). It has also been observed to segregate with disease in related individuals. This variant is also known as NM_001278464.1:c.385_386del (p.Glu129Lys*6). ClinVar contains an entry for this variant (Variation ID: 253264). For these reasons, this variant has been classified as Pathogenic. |
Gene |
RCV001854933 | SCV005080645 | pathogenic | not provided | 2024-02-20 | criteria provided, single submitter | clinical testing | Frameshift variant predicted to result in protein truncation or nonsense mediated decay in a gene for which loss of function is a known mechanism of disease; This variant is associated with the following publications: (PMID: 26825290, 33742459, 35982159, 35562572, 34573276, 29877124, 33718295, 35741050, 27328748) |
OMIM | RCV000239652 | SCV000298167 | pathogenic | Encephalopathy, lethal, due to defective mitochondrial peroxisomal fission 1 | 2016-08-25 | no assertion criteria provided | literature only |