IEMbase 0603: NUS1-related Nogo-B receptor deficiency
Scope
| Field | Value |
|---|---|
| IEMbase ID | 603 |
| Nosology | 18.4.02.02 |
| Gene | NUS1 |
| External IDs | OMIM:617082; ORPHA:442835 |
| Generated mapping | UNMAPPED; best candidate Generalized_Epilepsy_with_Febrile_Seizures_Plus.yaml#GABRD |
| Candidate DisMech targets | None exact |
| Review date | 2026-07-07 |
IEMbase phenotype signal
IEMbase represents NUS1-related Nogo-B receptor deficiency, labelled NUS1-CDG and NgBR-CDG. The record is autosomal recessive, classified under disorders of multiple glycosylation pathways, has unknown treatability, and has no treatment rows.
There are no biochemical rows. Clinical rows include neonatal or infantile axial hypotonia, cortical atrophy on MRI, developmental delay, epilepsy, failure to thrive, microcephaly, retinitis pigmentosa, scoliosis, and acral spasticity.
DisMech phenotype coverage
Generalized_Epilepsy_with_Febrile_Seizures_Plus.yaml#GABRD is a weak
false-positive candidate. It models GABRD/GABA-A receptor delta contribution to
GEFS+ and neuronal excitation-inhibition imbalance. It does not represent NUS1,
Nogo-B receptor / cis-prenyltransferase complex biology, autosomal recessive
CDG, retinitis pigmentosa, cortical atrophy, microcephaly, scoliosis, or the
failure-to-thrive phenotype bundle.
The local knowledge base has retinitis-pigmentosa and epilepsy modules/entries, but no exact NUS1-CDG target was identified.
Concordance and completeness
Judgement: true local gap; reject the GABRD epilepsy candidate.
The generated weak candidate reflects seizure vocabulary only. IEMbase centers a NUS1 glycosylation/dolichol-related neuroretinal syndrome with developmental and growth features, which is not covered by the local GEFS+ entry.
Curation actions
- Create or identify an exact NUS1 / Nogo-B receptor deficiency / NgBR-CDG target before import.
- Reject
Generalized_Epilepsy_with_Febrile_Seizures_Plus.yaml#GABRDas an exact mapping. - Preserve cortical atrophy, retinitis pigmentosa, epilepsy, microcephaly, axial hypotonia, acral spasticity, scoliosis, developmental delay, and failure-to-thrive prompts.