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| Home > In process > Loss-of-function variants in the CAPN1 activator CD99L2 cause X-linked spastic ataxia. > print |
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| 024 | 7 | _ | |a 10.1038/s41467-026-69337-9 |2 doi |
| 024 | 7 | _ | |a pmid:41690933 |2 pmid |
| 037 | _ | _ | |a DZNE-2026-00201 |
| 041 | _ | _ | |a English |
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| 100 | 1 | _ | |a Menden, Benita |b 0 |
| 245 | _ | _ | |a Loss-of-function variants in the CAPN1 activator CD99L2 cause X-linked spastic ataxia. |
| 260 | _ | _ | |a [London] |c 2026 |b Springer Nature |
| 336 | 7 | _ | |a article |2 DRIVER |
| 336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1771406565_1928 |2 PUB:(DE-HGF) |
| 336 | 7 | _ | |a ARTICLE |2 BibTeX |
| 336 | 7 | _ | |a JOURNAL_ARTICLE |2 ORCID |
| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 520 | _ | _ | |a Most patients with a rare movement disorder (MD) do not receive a molecular diagnosis, and the underlying genetic variants and mediating genes remain elusive. Here, we evaluate the diagnostic accuracy of conventional and next-generation sequencing-based genetic testing strategies in a cohort of 2,811 individuals with ataxia, spastic paraplegia and dystonia. Exome sequencing establishes genetic diagnoses in 19.3% of cases, and specificity of phenotypic features and age at testing are positive predictors. Genome analysis 'beyond the exome' increases the diagnostic yield by 7.5%, mostly due to the improved detection of structural variants and repeat expansions. Unsolved cases are included in the Solve-RD cohort and subjected to gene-burden analysis, providing evidence for loss-of-function variants in X-chromosomal CD99L2 causing spastic ataxia. Cellular studies show that the transmembrane protein CD99L2 occurs mainly in a ubiquitinated form and serves as an activating interactor of the calcium-dependent protease CAPN1. Ablation of cytoplasmic or extracellular domains of CD99L2 leads to its intracellular mislocalization and abrogation of its interplay with CAPN1. Transcriptome analysis in CD99L2 patient-derived fibroblasts reveals synaptic function-specific disturbances. Impaired CAPN1 activation and dysregulation of downstream neuronal pathways constitute the likely molecular cause for neurodegeneration. |
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| 650 | _ | 7 | |a Calpain |0 EC 3.4.22.- |2 NLM Chemicals |
| 650 | _ | 7 | |a CAPN1 protein, human |0 EC 3.4.22.52 |2 NLM Chemicals |
| 650 | _ | 7 | |a 12E7 Antigen |2 NLM Chemicals |
| 650 | _ | 2 | |a Humans |2 MeSH |
| 650 | _ | 2 | |a Calpain: metabolism |2 MeSH |
| 650 | _ | 2 | |a Calpain: genetics |2 MeSH |
| 650 | _ | 2 | |a Muscle Spasticity: genetics |2 MeSH |
| 650 | _ | 2 | |a Muscle Spasticity: diagnosis |2 MeSH |
| 650 | _ | 2 | |a Muscle Spasticity: metabolism |2 MeSH |
| 650 | _ | 2 | |a Spinocerebellar Ataxias: genetics |2 MeSH |
| 650 | _ | 2 | |a Spinocerebellar Ataxias: diagnosis |2 MeSH |
| 650 | _ | 2 | |a Spinocerebellar Ataxias: metabolism |2 MeSH |
| 650 | _ | 2 | |a Male |2 MeSH |
| 650 | _ | 2 | |a Female |2 MeSH |
| 650 | _ | 2 | |a 12E7 Antigen: genetics |2 MeSH |
| 650 | _ | 2 | |a 12E7 Antigen: metabolism |2 MeSH |
| 650 | _ | 2 | |a Optic Atrophy: genetics |2 MeSH |
| 650 | _ | 2 | |a Optic Atrophy: diagnosis |2 MeSH |
| 650 | _ | 2 | |a Adult |2 MeSH |
| 650 | _ | 2 | |a Loss of Function Mutation |2 MeSH |
| 650 | _ | 2 | |a Exome Sequencing |2 MeSH |
| 650 | _ | 2 | |a Adolescent |2 MeSH |
| 650 | _ | 2 | |a Cohort Studies |2 MeSH |
| 650 | _ | 2 | |a Fibroblasts: metabolism |2 MeSH |
| 650 | _ | 2 | |a Child |2 MeSH |
| 650 | _ | 2 | |a Middle Aged |2 MeSH |
| 650 | _ | 2 | |a Genetic Testing |2 MeSH |
| 650 | _ | 2 | |a Genetic Diseases, X-Linked: genetics |2 MeSH |
| 650 | _ | 2 | |a Genetic Diseases, X-Linked: diagnosis |2 MeSH |
| 650 | _ | 2 | |a Young Adult |2 MeSH |
| 650 | _ | 2 | |a Intellectual Disability |2 MeSH |
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