Intracellular C1q - an unexpected player in neuronal proteostasis.

Autor: West EE; Complement and Inflammation Research Section, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA. Electronic address: erin.west@nih.gov., Kemper C; Complement and Inflammation Research Section, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA. Electronic address: claudia.kemper@nih.gov.
Jazyk: angličtina
Zdroj: Trends in immunology [Trends Immunol] 2024 Oct; Vol. 45 (10), pp. 718-720. Date of Electronic Publication: 2024 Sep 25.
DOI: 10.1016/j.it.2024.09.006
Abstrakt: Extrahepatic, cell-autonomous, and/or intracellularly active complement components are increasingly recognized as key orchestrators of cell physiological processes. A recent study by Scott-Hewitt et al. demonstrates that microglia-derived C1q unexpectedly associates with the ribosomes of neurons in the aging murine brain, where it impacts protein translation and impairs the extinction of conditioned fear responses.
Competing Interests: Declaration of interests The authors declare no competing interests.
(Published by Elsevier Ltd.)
Databáze: MEDLINE
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