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G protein regulation of neuronal calcium channels: back to the future
J. Proft, N. Weiss,
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články, práce podpořená grantem, přehledy
NLK
Open Access Digital Library
od 1965-07-01
Open Access Digital Library
od 1997-01-01
ROAD: Directory of Open Access Scholarly Resources
PubMed
25549669
DOI
10.1124/mol.114.096008
Knihovny.cz E-zdroje
- MeSH
- blokátory kalciových kanálů farmakologie MeSH
- konformace proteinů MeSH
- lidé MeSH
- neurony metabolismus MeSH
- presynaptická zakončení metabolismus MeSH
- proteiny vázající GTP - beta-podjednotky metabolismus MeSH
- proteiny vázající GTP - gama-podjednotky metabolismus MeSH
- proteiny vázající GTP metabolismus MeSH
- receptory spřažené s G-proteiny metabolismus MeSH
- vápníkové kanály chemie metabolismus MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
Neuronal voltage-gated calcium channels have evolved as one of the most important players for calcium entry into presynaptic endings responsible for the release of neurotransmitters. In turn, and to fine-tune synaptic activity and neuronal communication, numerous neurotransmitters exert a potent negative feedback over the calcium signal provided by G protein-coupled receptors. This regulation pathway of physiologic importance is also extensively exploited for therapeutic purposes, for instance in the treatment of neuropathic pain by morphine and other μ-opioid receptor agonists. However, despite more than three decades of intensive research, important questions remain unsolved regarding the molecular and cellular mechanisms of direct G protein inhibition of voltage-gated calcium channels. In this study, we revisit this particular regulation and explore new considerations.
Citace poskytuje Crossref.org
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- $a Neuronal voltage-gated calcium channels have evolved as one of the most important players for calcium entry into presynaptic endings responsible for the release of neurotransmitters. In turn, and to fine-tune synaptic activity and neuronal communication, numerous neurotransmitters exert a potent negative feedback over the calcium signal provided by G protein-coupled receptors. This regulation pathway of physiologic importance is also extensively exploited for therapeutic purposes, for instance in the treatment of neuropathic pain by morphine and other μ-opioid receptor agonists. However, despite more than three decades of intensive research, important questions remain unsolved regarding the molecular and cellular mechanisms of direct G protein inhibition of voltage-gated calcium channels. In this study, we revisit this particular regulation and explore new considerations.
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