Lactylation as a post-translational regulator of cGAS and immunity.
| Autor: | Liu H; Shanghai Key Laboratory of Tuberculosis, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China; Key Laboratory of Pathogen-Host Interaction, Ministry of Education, Department of Microbiology and Immunology, Tongji University School of Medicine, Shanghai, China; Clinical Translation Research Center, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China. Electronic address: haipengliu@tongji.edu.cn., Ge B; Shanghai Key Laboratory of Tuberculosis, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China; Key Laboratory of Pathogen-Host Interaction, Ministry of Education, Department of Microbiology and Immunology, Tongji University School of Medicine, Shanghai, China; Clinical Translation Research Center, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China. Electronic address: gebaoxue@sibs.ac.cn. |
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| Jazyk: | angličtina |
| Zdroj: | Molecular cell [Mol Cell] 2024 Dec 05; Vol. 84 (23), pp. 4483-4485. |
| DOI: | 10.1016/j.molcel.2024.11.018 |
| Abstrakt: | In a recent paper at Nature, Li et al. 1 reported that alanine-tRNA synthetases AARS1 and AARS2 are lactate sensors and mediate lactylation of cGAS, leading to its inactivation. Competing Interests: Declaration of interests The authors declare no competing interests. (Copyright © 2024 Elsevier Inc. All rights reserved.) |
| Databáze: | MEDLINE |
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