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Allosteric modulation of A(3) adenosine receptors by a series of 3-(2-pyridinyl)isoquinoline derivatives.
- Z. Gao, J. V. van Muijlwijk-Koezen, A. Chen, C. Müller, A. IJzerman, K. Jacobson
- Chemistry, MedicineMolecular pharmacology
- 1 November 2001
Probing of structure-activity relationships suggested that a carbonyl group is essential for allosterism but preferred only for competitive antagonism, suggesting that the structural requirements forallosteric enhancement might be distinct from those forcompetitive antagonism.
Allosteric modulation of A(2A) adenosine receptors by amiloride analogues and sodium ions.
The slopes of the HMA concentration-response curves in the presence and absence of sodium ions were not significantly different, which suggests that sodium ions and amiloride analogues act at a common allosteric site on the A(2A) adenosine receptor.
Neoceptor concept based on molecular complementarity in GPCRs: a mutant adenosine A(3) receptor with selectively enhanced affinity for amine-modified nucleosides.
- K. Jacobson, Z. Gao, +7 authors B. Liang
- Chemistry, MedicineJournal of medicinal chemistry
- 22 November 2001
The human A(3) receptor is mutated at the site of a critical His residue in TM7, previously proposed to be involved in ligand recognition through interaction with the ribose moiety, to create a unique receptor mutant that would be activated by tailor-made synthetic ligands.
The A3 adenosine receptor agonist CF502 inhibits the PI3K, PKB/Akt and NF-kappaB signaling pathway in synoviocytes from rheumatoid arthritis patients and in adjuvant-induced arthritis rats.
Taken together, CF502 inhibits FLS growth and the inflammatory manifestations of arthritis, supporting the development of A(3)AR agonists for the treatment of rheumatoid arthritis.
Anti-nicotinic properties of anticholinergic antiparkinson drugs.
- Z. Gao, B. Y. Liu, W. Cui, L. Li, Q. Fan, C. Liu
- MedicineThe Journal of pharmacy and pharmacology
The experiments demonstrate that the anticholinergic antiparkinson drugs and mecamylamine effectively antagonize nicotine- induced convulsion, but atropine does not; some of these drugs have competitive properties whereas others seem to have both competitive and non-competitive properties in antagonizing nicotine-induced convulsion in mice.
Site-directed mutagenesis studies of human A(2A) adenosine receptors: involvement of glu(13) and his(278) in ligand binding and sodium modulation.
- Z. Gao, Q. Jiang, K. Jacobson, A. IJzerman
- Chemistry, MedicineBiochemical pharmacology
- 1 September 2000
The results suggest that the two closely linked residues Glu13 and His278 in A(2A) adenosine receptor are most important for agonist recognition and are partly responsible for the allosteric regulation by sodium ions.
Pharmacology: Anti‐nicotinic Properties of Anticholinergic Antiparkinson Drugs
The nature of the antagonism by anticholinergic compounds of nicotine‐induced convulsion in mice has not been defined clearly. Although, because they do not compete effectively for agonist binding to…
Constitutive activation of A(3) adenosine receptors by site-directed mutagenesis.
The results indicated that specific locations within the TMs proximal to the cytosolic region were responsible for constraining the receptor in a G protein-uncoupled conformation.
Effects of nicotine on 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine-induced depression of striatal dopamine content and spontaneous locomotor activity in C57 black mice.
It was demonstrated that the lethal effect of MPTP was also partly protected by the chronic Nicotine treatment, and the chronic nicotine treatment also significantly protected MPTP-depressed spontaneous locomotor activity in mice.
Expression of gaba transaminase immunoreactivity in interneurons of the rat neostriatum
- K. Yung, K. Kwok, Z. Gao, S. Choi, F. Kwok
- Biology, MedicineNeurochemistry International
- 1 December 1998
The present results indicate the GABAergic interneurons in the neostriatum and a subpopulation of pallidal neurons play an important role in metabolic degradation of GABA in the basal ganglia.