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  1. Article ; Online: Involvement of the L-DOPA receptor GPR143 in acute and chronic actions of methylphenidate.

    Uchimura, Hiraku / Kanai, Kaori / Arai, Masami / Inoue, Miyu / Hishimoto, Akitoyo / Masukawa, Daiki / Goshima, Yoshio

    Journal of pharmacological sciences

    2023  Volume 152, Issue 3, Page(s) 178–181

    Abstract: Methylphenidate (MPH) and methamphetamine (METH) are the current treatments of choice for attention deficit/hyperactivity disorder. We previously reported that METH induces the release of dopamine (DA) and of the neurotransmitter candidate L-3,4- ... ...

    Abstract Methylphenidate (MPH) and methamphetamine (METH) are the current treatments of choice for attention deficit/hyperactivity disorder. We previously reported that METH induces the release of dopamine (DA) and of the neurotransmitter candidate L-3,4-dihydroxyphenylalanine (L-DOPA). In contrast, we here found that MPH increased the DA release while it did not affect the L-DOPA release from the dorsolateral striatum. Nevertheless, MPH-induced hyperlocomotion was reduced in Gpr143 (L-DOPA receptor) gene-deficient (Gpr143
    MeSH term(s) Mice ; Animals ; Methylphenidate/pharmacology ; Levodopa/pharmacology ; Receptors, Neurotransmitter ; Dopamine/metabolism ; Methamphetamine/pharmacology ; Central Nervous System Stimulants/pharmacology
    Chemical Substances Methylphenidate (207ZZ9QZ49) ; levodopa receptor ; Levodopa (46627O600J) ; Receptors, Neurotransmitter ; Dopamine (VTD58H1Z2X) ; Methamphetamine (44RAL3456C) ; Central Nervous System Stimulants
    Language English
    Publishing date 2023-04-28
    Publishing country Japan
    Document type Journal Article
    ZDB-ID 2104264-0
    ISSN 1347-8648 ; 1347-8613
    ISSN (online) 1347-8648
    ISSN 1347-8613
    DOI 10.1016/j.jphs.2023.04.006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: SARS-CoV-2 Spike Protein Mutation at Cysteine-488 Impairs Its Golgi Localization and Intracellular S1/S2 Processing.

    Yamamoto, Yuichiro / Inoue, Tetsuya / Inoue, Miyu / Murae, Mana / Fukasawa, Masayoshi / Kaneko, Mika K / Kato, Yukinari / Noguchi, Kohji

    International journal of molecular sciences

    2022  Volume 23, Issue 24

    Abstract: The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike protein binds to the cellular receptor-angiotensin-converting enzyme-2 (ACE2) as the first step in viral cell entry. SARS-CoV-2 spike protein expression in the ACE2-expressing cell ... ...

    Abstract The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike protein binds to the cellular receptor-angiotensin-converting enzyme-2 (ACE2) as the first step in viral cell entry. SARS-CoV-2 spike protein expression in the ACE2-expressing cell surface induces cell-cell membrane fusion, thus forming syncytia. To exert its fusogenic activity, the spike protein is typically processed at a specific site (the S1/S2 site) by cellular proteases such as furin. The C488 residue, located at the spike-ACE2 interacting surface, is critical for the fusogenic and infectious roles of the SARS-CoV-2 spike protein. We have demonstrated that the C488 residue of the spike protein is involved in subcellular targeting and S1/S2 processing. C488 mutant spike localization to the Golgi apparatus and cell surface were impaired. Consequently, the S1/S2 processing of the spike protein, probed by anti-Ser-686-cleaved spike antibody, markedly decreased in C488 mutant spike proteins. Moreover, brefeldin-A-mediated endoplasmic-reticulum-to-Golgi traffic suppression also suppressed spike protein S1/S2 processing. As brefeldin A treatment and C488 mutation inhibited S1/S2 processing and syncytia formation, the C488 residue of spike protein is required for functional spike protein processing.
    Language English
    Publishing date 2022-12-13
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms232415834
    Database MEDical Literature Analysis and Retrieval System OnLINE

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