Počet záznamů: 1  

SGIP1 in axons prevents internalization of desensitized CB1R and modifies its function

  1. 1.
    SYSNO ASEP0575884
    Druh ASEPJ - Článek v odborném periodiku
    Zařazení RIVJ - Článek v odborném periodiku
    Poddruh JČlánek ve WOS
    NázevSGIP1 in axons prevents internalization of desensitized CB1R and modifies its function
    Tvůrce(i) Durydivka, Oleh (UMG-J)
    Mackie, K. (US)
    Blahoš, Jaroslav (UMG-J) RID
    Celkový počet autorů3
    Číslo článku1213094
    Zdroj.dok.Frontiers in Neuroscience
    Roč. 17, Jul (2023)
    Poč.str.11 s.
    Jazyk dok.eng - angličtina
    Země vyd.CH - Švýcarsko
    Klíč. slovacannabinoid receptor 1 ; synaptic transmission ; axon enrichment ; clathrin-mediated endocytosis ; internalization
    Obor OECDBiochemistry and molecular biology
    CEPGA19-24172S GA ČR - Grantová agentura ČR
    GA21-02371S GA ČR - Grantová agentura ČR
    Způsob publikováníOpen access
    Institucionální podporaUMG-J - RVO:68378050
    UT WOS001039801200001
    EID SCOPUS85166532925
    DOI10.3389/fnins.2023.1213094
    AnotaceIn the central nervous system (CNS), cannabinoid receptor 1 (CB1R) is preferentially expressed in axons where it has a unique property, namely resistance to agonist-driven endocytosis. This review aims to summarize what we know about molecular mechanisms of CB1R cell surface stability in axonal compartments, how these impact CB1R signaling, and to consider their physiological consequences. This review then focuses on a potential candidate for maintaining axonal CB1R at the cell surface, Src homology 3-domain growth factor receptor-bound 2-like endophilin interacting protein 1 (SGIP1). SGIP1 may contribute to the polarized distribution of CB1R and modify its signaling in axons. In addition, deletion of SGIP1 results in discrete behavioral changes in modalities controlled by the endocannabinoid system in vivo. Several drugs acting directly via CB1R have important therapeutic potential, however their adverse effects limit their clinical use. Future studies might reveal chemical approaches to target the SGIP1-CB1R interaction, with the aim to exploit the endocannabinoid system pharmaceutically in a discrete way, with minimized undesired consequences.
    PracovištěÚstav molekulární genetiky
    KontaktNikol Škňouřilová, nikol.sknourilova@img.cas.cz, Tel.: 241 063 217
    Rok sběru2024
    Elektronická adresahttps://www.frontiersin.org/articles/10.3389/fnins.2023.1213094/full
Počet záznamů: 1  

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