ArticleMolecular brain2021
The novel multiple sclerosis susceptibility gene ATXN1 regulates B cell receptor signaling in B-1a cells.
Article in Molecular brain, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- Multiomics Profiling During Autoimmune Demyelination Highlights a Complex Regulatory Role for Ataxin-1 in B Cells.Annals of the New York Academy of Sciences · 2026Article
- Oligodendrocyte dysfunction contributes to motor deficits and Purkinje cell axonopathy in spinocerebellar ataxia type 1.The Journal of clinical investigation · 2026Article
- Conditional deletion of the multiple sclerosis susceptibility gene ATXN1 identifies cell-autonomous effects in the B-cell compartment.The FEBS journal · 2026Article
- An expanded polyglutamine in ATAXIN1 results in a loss-of-function that exacerbates severity of Multiple Sclerosis in an EAE mouse model.Journal of neuroinflammation · 2025Article
- Co-existence of Myelin Oligodendrocyte Glycoprotien Antibody-associated Disease (MOGAD) and Spinocerebellar Ataxia type 1 (SCA1): A case report.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024Article
- The epigenetic modification of DNA methylation in neurological diseases.Frontiers in immunology · 2024Review
- Epigenetic control of ataxin-1 in multiple sclerosis.Annals of clinical and translational neurology · 2022Article
- Prioritization of risk genes in multiple sclerosis by a refined Bayesian framework followed by tissue-specificity and cell type feature assessment.BMC genomics · 2022Article
- Genetics and functional genomics of multiple sclerosis.Seminars in immunopathology · 2022Review
- B-Cell and T-Cell Populations in Peripheral Blood Linked to Ocrelizumab Treatment Efficacy in Multiple Sclerosis.In vivo (Athens, Greece)Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple sclerosis (MS) is an autoimmune demyelinating disease of the central nervous system (CNS) caused by complex gene-environment interactions. ATXN1 maps to 6p22.3, within the 233 loci associated with an increased risk of developing MS. Toxic gain-of-function mutations in ATXN1 cause the neurodegenerative disorder spinocerebellar ataxia type 1 (SCA1). Conversely, ATXN1 loss-of-function is involved in Alzheimer's disease (AD) and tumorigenesis. We have recently shown that ATXN1 exerts a protective immunomodulatory activity in the MS model experimental autoimmune encephalomyelitis (EAE). Specifically, we demonstrated that mice lacking Atxn1 experience aggravated EAE due to aberrant B cell functions. Atxn1-null mice exhibit increased B cell proliferation with the concomitant expansion of specific B cell subsets including B-1a cells. This population of B cells is responsible for the production of natural immunoglobulins and has been associated with the etiology of multiple autoimmune diseases. To understand the role played by Atxn1 in these cells, we performed comprehensive transcriptomic profiling of Atxn1-null B-1a cells before and after stimulation with an encephalitogenic antigen. Importantly, we show that in this sub-population Atxn1 regulates immunoglobulin gene transcription and signaling through the B cell receptor (BCR).
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