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Modulation by mu-opioid agonists of guanosine-5'-O-(3-[35S]thio)triphosphate binding to membranes from human neuroblastoma SH-SY5Y cells.
The ability of mu-opioid agonists to activate G proteins has been demonstrated by studying the binding of the GTP analogue guanosine-5'-O-(3-[35S]thio)triphosphate ([35S]GTP gamma S) to membranesExpand
Non-visual GRKs: are we seeing the whole picture?
TLDR
Recent work has indicated roles for the other, non-visual GRKs and has revealed potential phosphorylation-independent regulation of GPCRs by GRK2 and GRK3, which is reviewed to attempt to put it into context withGRKs as physiological regulators that could be appropriate targets for future pharmacological intervention. Expand
Neuronal Ca2+ stores: activation and function
TLDR
Two mechanisms of release of Ca2+ enable considerable temporal and spatial complexity of increases in the [Ca2+]i via multiple interactions at the level of intracellular-receptor activation, which underlie mechanisms that are central to information transfer and integration within neuronal compartments. Expand
Differential Regulation of Muscarinic Acetylcholine Receptor-sensitive Polyphosphoinositide Pools and Consequences for Signaling in Human Neuroblastoma Cells*
TLDR
The basal turnover of phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2) and M3-muscarinic receptor-mediated changes in phosphoinositides in the human neuroblastoma cell line, SH-SY5Y is quantitatively assessed. Expand
The muscarinic M5 receptor: a silent or emerging subtype?
TLDR
Current data on the muscarinic receptor M5 subtype is critically evaluated to stimulate further studies on the M5 receptor that may raise it from a 'relatively ephemeral' or 'fact or fiction' status, described in recent reviews. Expand
Determinants of Metabotropic Glutamate Receptor-5-mediated Ca2+ and Inositol 1,4,5-Trisphosphate Oscillation Frequency
TLDR
A single receptor can stimulate two types of InsP3-mediated Ca2+ signal dependent upon feedback inhibition, producing two distinct means of controlling the final pattern of Ca2- i release. Expand
New developments in the molecular pharmacology of the myo-inositol 1,4,5-trisphosphate receptor.
TLDR
Recent developments in IP3 receptor pharmacology are reviewed, with particular emphasis on ligand molecular recognition by this receptor-channel complex, and the potential for designing non-inositol phosphate-based agonists and antagonists is discussed. Expand
Lithium and the phosphoinositide cycle: an example of uncompetitive inhibition and its pharmacological consequences.
TLDR
Stefan Nahorski, Ian Ragan and John Challiss discuss this unusual stimulus-dependent form of enzyme inhibition, emphasizing that the selectivity exhibited by lithium depends upon the degree of inositol lipid hydrolysis and polyphosphoinositide dephosphorylation. Expand
Muscarinic receptor activation down-regulates the type I inositol 1,4,5-trisphosphate receptor by accelerating its degradation.
TLDR
In conclusion, phosphoinositidase C-linked muscarinic receptors down-regulate the type I InsP3 receptor by accelerating its degradation, and it appears that this process is initiated by persistent discharge of intracellular Ca2+ stores via the channels formed by tetramerically complexed type I insP3 receptors. Expand
Lack of a C-terminal Tail in the Mammalian Gonadotropin-releasing Hormone Receptor Confers Resistance to Agonist-dependent Phosphorylation and Rapid Desensitization*
TLDR
It is demonstrated that the lack of a C-terminal tail in the mammalian GnRH-R results in an inability of the receptor to undergo agonist-dependent phosphorylation and that this results directly in a resistance to rapid desensitization. Expand
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