ArticleProceedings of the National Academy of Sciences of the United States of America2023
Causal ALS genes impact the MHC class II antigen presentation pathway.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- HMC3 revealed: how much do these "Microglia" really tell us?Frontiers in immunology · 2026Review
- Classical HLA class II associations with ALS in Kuwait reveal a DR7-DQ2.2 risk haplotype.Frontiers in immunology · 2026Article
- Article
- Myeloid antigen-presenting cells in neurodegenerative diseases: a focus on classical and non-classical MHC molecules.Frontiers in neuroscience · 2024Review
- Linking ALS mutations to the disruption of the MHC-II pathway.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
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Abstract
Mutations in RNA/DNA-binding proteins cause amyotrophic lateral sclerosis (ALS), but the underlying disease mechanisms remain unclear. Here, we report that a set of ALS-associated proteins, namely FUS, EWSR1, TAF15, and MATR3, impact the expression of genes encoding the major histocompatibility complex II (MHC II) antigen presentation pathway. Both subunits of the MHC II heterodimer, HLA-DR, are down-regulated in ALS gene knockouts/knockdown in HeLa and human microglial cells, due to loss of the MHC II transcription factor CIITA. Importantly, hematopoietic progenitor cells (HPCs) derived from human embryonic stem cells bearing the FUS
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