ArticleCell discovery2024
LncRNA TubAR complexes with TUBB4A and TUBA1A to promote microtubule assembly and maintain myelination.
Article in Cell discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- Research Progress on Spinal Cord Repair Based on Regulation of the Neuroregenerative Microenvironment.Cellular and molecular neurobiology · 2026Review
- Transcriptome combined with single-cell data to construct a prognostic model for glycosylation-related genes in osteosarcoma.Discover oncology · 2026Article
- Pathological mechanisms of motor dysfunction in familial Danish dementia: insights from a knock-in rat model.Journal of neuroinflammation · 2025Article
- The lncRNA MYRACL regulates human oligodendrocyte maturation and myelination.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Insights into organelle forming RNAs: Diversity, functions and future perspectives.Animal models and experimental medicine · 2025Review
- New insights into mitochondrial segregation from the Doubly Uniparental Inheritance system in bivalves.BMC biology · 2025Article
- Unraveling the advances of non-coding RNAs on the tumor microenvironment: innovative strategies for cancer therapies.Journal of translational medicine · 2025Review
- Multi-Omics Analysis of Hippocampus in Rats Administered Trimethyltin Chloride.Neurotoxicity research · 2025Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
A long-standing hypothesis proposes that certain RNA(s) must exhibit structural roles in microtubule assembly. Here, we identify a long noncoding RNA (TubAR) that is highly expressed in cerebellum and forms RNA-protein complex with TUBB4A and TUBA1A, two tubulins clinically linked to cerebellar and myelination defects. TubAR knockdown in mouse cerebellum causes loss of oligodendrocytes and Purkinje cells, demyelination, and decreased locomotor activity. Biochemically, we establish the roles of TubAR in promoting TUBB4A-TUBA1A heterodimer formation and microtubule assembly. Intriguingly, different from the hypomyelination-causing mutations, the non-hypomyelination-causing mutation TUBB4A-R2G confers gain-of-function for an RNA-independent interaction with TUBA1A. Experimental use of R2G/A mutations restores TUBB4A-TUBA1A heterodimer formation, and rescues the neuronal cell death phenotype caused by TubAR knockdown. Together, we uncover TubAR as the long-elusive structural RNA for microtubule assembly and demonstrate how TubAR mediates microtubule assembly specifically from αβ-tubulin heterodimers, which is crucial for maintenance of cerebellar myelination and activity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.