ArticleCell communication and signaling : CCS2025
CARM1 regulates tubulin autoregulation through PI3KC2α R175 methylation.
Article in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- KDM4A Erases the H3R17me2a Mark, Facilitating Chromosome Condensation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Protein arginine methyltransferases in cancer: mechanisms, functions, and therapeutic opportunities.Journal of biomedical science · 2026Review
- Reversible arginine methylation regulates mitochondrial IDH2 activity: coordinated control by CARM1 and KDM3A/4A.Cell death & disease · 2026Article
- Multilayered regulation of cytoskeletal protein abundance: autoregulatory mechanisms of actin and tubulin.Experimental & molecular medicine · 2026Review
- Context-specific applications of CARM1 inhibitors: functional profiles of EZM2302 and TP-064.Molecular medicine (Cambridge, Mass.) · 2025Article
- Reversible arginine methylation of PI3KC2α controls mitotic spindle dynamics.Cell communication and signaling : CCS · 2025Article
- Multifaceted roles of CARM1 beyond histone arginine methylation.Experimental & molecular medicine · 2025Review
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Authors and funding
6 authors.
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Abstract
Tubulin is crucial in several cellular processes, including intracellular organization, organelle transport, motility, and chromosome segregation. Intracellular tubulin concentration is tightly regulated by an autoregulation mechanism, in which excess free tubulin promotes tubulin mRNA degradation. However, the details of how changes in free tubulin levels initiate this autoregulation remain unclear. In this study, we identified coactivator-associated arginine methyltransferase 1 (CARM1)-phosphatidylinositol 3-kinase class 2α (PI3KC2α) axis as a novel regulator of tubulin autoregulation. CARM1 stabilizes PI3KC2α by methylating its R175 residue. Once PI3KC2α is not methylated, it becomes unstable, leading to decreased cellular levels. Loss of PI3KC2α results in the release of tetratricopeptide repeat domain 5 (TTC5), which initiates tubulin autoregulation. Thus, PI3KC2α, along with its CARM1-mediated arginine methylation, regulates the initiation of tubulin autoregulation. Additionally, disruption of the CARM1-PI3KC2α axis decreases intracellular tubulin levels, leading to a synergistic increase in the cytotoxicity of microtubule-targeting agents (MTAs). Taken together, our study demonstrates that the CARM1-PI3KC2α axis is a key regulator of TTC5-mediated tubulin autoregulation and that disrupting this axis enhances the anti-cancer activity of MTAs.
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