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1 tent with the activation of ocular adenosine A2 receptors.
2 lly reversed by blockade of adenosine A1 and A2 receptors.
3 .g., human platelet thrombin and thromboxane A2 receptors.
4  increase in Galphaq coupling to thromboxane A2 receptors.
5 n increase in ligand affinity of thromboxane A2 receptors.
6 tinguishable from human platelet thromboxane A2 receptors.
7 may mediate the desensitization of adenosine A2 receptors.
8  podocyte antigens: the M-type phospholipase A2 receptor 1 (PLA2R) and thrombospondin type 1 domain-c
9                                Phospholipase A2 receptor 1 (PLA2R) is a target autoantigen in 70% of
10 ive until 2009 when the M-type phospholipase A2 receptor 1 (PLA2R) was identified as a disease autoan
11 jor target antigen, the M-type phospholipase A2 receptor 1 (PLA2R).
12  the podocyte surface antigens phospholipase A2 receptor 1 (PLA2R1) and the recently identified throm
13                                Phospholipase A2 receptor 1 (PLA2R1) is a 180-kDa transmembrane protei
14 ) along with the major antigen phospholipase A2 receptor 1 (PLA2R1).
15 ith autoantibodies against the phospholipase A2 receptor 1 (PLA2R1).
16 us nephropathy target antigens phospholipase A2 receptor 1 and thrombospondin type 1 domain-containin
17 ntibodies targeting the M-type phospholipase A2 receptor-1 (PLA2R) on the surface of glomerular visce
18 clinical scenario, focusing on phospholipase A2 receptor; ( 2 ) one antigen!=one clinical condition,
19  the ortholog of the mammalian phospholipase A2 receptor, a mannose receptor family member, rather th
20 In the central nervous system, noradrenergic a2 receptors (a2-ARs) are widely expressed in the motor
21                           DPMA, an adenosine A2 receptor (A2R) agonist, decreased KDR mRNA in a dose-
22 imulatory concentrations; however, adenosine A2 receptor (A2R) agonists DPMA, NECA, and CGS21680 incr
23 or prosurvival GsPCRs, we explored adenosine-A2-receptor (A2R), CGRPR (calcitonin-gene-related-peptid
24 5'-(N-ethylcalboxamido)-adenosine (adenosine A2 receptor [A2R] agonists, Kd = 15 and 16 nmol/l, respe
25 on of PKC can block the effects of adenosine A2 receptor activation by CGS-21680 on anoxia and reoxyg
26  A1 receptor activation, the implications of A2 receptor activation on synaptic transmission have not
27 d which inhibits neutrophil function through A2 receptor activation.
28                                The adenosine A2 receptor agonist 5'-(N-cyclopropyl)-carboxamidoadenos
29  stimulated O2.- generation by the adenosine A2 receptor agonist 5'-N-ethylcarboxamidoadenosine (NECA
30                      The selective adenosine A2 receptor agonist DPMA (10 micromol/L) decreased TNF-a
31 an platelets by thrombin and the thromboxane A2 receptor agonist U46619 lead to phosphorylation of Ga
32  vasoconstriction induced by the thromboxane A2 receptor agonist U46619, which suggest a NO-independe
33 enosine (CGS-21680 [20 nmol/L], an adenosine A2 receptor agonist, R-(--)-N6-(2-phenylisopropyl)-adeno
34 ated by adenosine (10 microM, 2 min) and the A2-receptor agonist 2-p-(2-carboxyethyl)phenethylamino-5
35                 Reactivity for phospholipase A2 receptor and thrombospondin type 1 domain containing
36     The effect appears to be mediated by the A2 receptor and transduced through a G protein-adenylyl
37 demonstrated expression of the phospholipase A2 receptor and two G-protein-coupled receptors for LPC
38 y requires adenosine activation of adenosine A2 receptors and is mediated by beta gamma dimers.
39 acting to increase O2 delivery via adenosine A2 receptors and to decrease metabolic rate via A1 recep
40               In contrast, a highly specific A2 receptor antagonist (10(-7) or 10(-5) M) had no effec
41 yl-1, 3-dipropylxanthine (DPCPX) but not the A2 receptor antagonist 3, 7-dimethyl-1-propargylxanthine
42  or inhibition of adenosine by the adenosine A2 receptor antagonist 3,7-dimethyl-1-propargylxanthine
43 nists and AP-5 were reversed by an adenosine A2 receptor antagonist administered intraperitoneally.
44 lished by administration of the adenosine A1/A2 receptor antagonist PD 115,199 (3 mg/kg i.v.) before
45                  Aspirin and the thromboxane A2 receptor antagonist SQ29548 inhibited activation of t
46      After pretreatment with the thromboxane A2 receptor antagonist SQ30, 741, the vasoconstrictor re
47 ected by 3,7-dimethy-1-propargylxanthine, an A2 receptor antagonist.
48 se of ticagrelor followed by an adenosine A1/A2-receptor antagonist [8-(p-sulfophenyl)theophylline, 4
49 ase, in the presence of the adenosine A1 and A2 receptor antagonists 8-cyclopentyl-1,3-dipropylxanthi
50 r agonist CGS-21680 (50% closure by day 2 in A2 receptor antagonists.
51 of L-arginine transport was inhibited by the A2-receptor antagonists ZM-241385 and 3,7-dimethyl-1-pro
52 hyl ester (an NO synthase inhibitor) and the A2-receptor antagonists ZM-241385 and DMPX prevented inc
53 circulating nephritogenic anti-phospholipase A2 receptor (anti-PLA2R) autoantibodies and genetic poly
54 most cases associated with anti-phospholipid A2 receptor antibodies (antiPLA2R).
55 P = 0.010] and those with anti-phospholipase A2 receptor antibodies [hazard ratio = 3.761 (1.635-8.65
56  most cases associated with antiphospholipid A2 receptor antibodies.
57                   Rates of antiphospholipase A2 receptor antibody (anti-PLA2R-Ab) depletion in NIAT-r
58 active against a polyclonal anti-thromboxane A2 receptor antibody.
59 riments tested the hypothesis that adenosine A2 receptors are involved in central reward function.
60                           Anti-phospholipase A2 receptor autoantibody (PLA2R-Ab) plays a critical rol
61                                              A2 receptor blockade by the A2 antagonist, DMPX (3,7-dim
62                                              A2 receptor blockade in the presence of complete A1 rece
63 nase inhibition with aspirin and thromboxane A2 receptor blockade with ifetroban on the chronic vasod
64                              D2 or adenosine A2 receptor blockade, pertussis toxin, Rp-cAMPS, or over
65  EP4, prostaglandin F2alpha, and thromboxane A2 receptors but not anti-inflammatory EP2, prostaglandi
66 onists, including caffeine, or targeting the A2 receptors by siRNA pretreatment of T cells improved t
67 uency test pulses (0.033 Hz) indicating that A2 receptors can enhance synaptic transmission.
68                             Agents active at A2 receptors either were without effect or could be bloc
69        The erythropoietin-producing hepatoma A2 receptor (EphA2) is a tyrosine kinase overexpressed b
70 nd activation of the signal molecules ephrin-A2 receptor, FAK, Src, and Rac1.
71 ntegrin molecules and tyrosine kinase ephrin-A2 receptor, followed by the activation of preexisting i
72                                              A2 receptors for extracellular adenosine might act as bo
73 ate the presence of a functional thromboxane A2 receptor in oligodendrocytes and are consistent with
74 ons indicating a high density of thromboxane A2 receptors in myelinated brain and spinal cord fiber t
75       The presence of functional thromboxane A2 receptors in neonatal rat oligodendrocytes and human
76               The human platelet thromboxane A2 receptor is a member of the G-protein-coupled superfa
77  increase of the transmembrane Ectodysplasin-A2-Receptor is a prominent tissue-independent alteration
78 oward the extracellular domain of the ephrin A2 receptor, long circulation half-life (8-12 h) in mous
79     Together, these results suggest that the A2 receptors may play an important role in the induction
80  the protective effects of adenosine include A2-receptor mediated vasodilation, A1-receptor mediated
81 y of the novel antagonist N-0861, the A1 and A2 receptor-mediated cardiac effects of adenosine were i
82  8-chlorostyrylcaffeine (CSC), suggesting an A2 receptor-mediated mechanism.
83 nstriction in vivo, which is often masked by A2 receptor-mediated vasodilation.
84 ed NDNF, while IgG eluate from phospholipase A2 receptor-MN showed no binding.
85 50 cases (discovery cohort) of phospholipase A2 receptor-negative MN to identify novel target antigen
86      Donor-derived MN is rare, phospholipase A2 receptor-negative, and can still be encountered in li
87 tis or antinephrin/anti-M-type phospholipase A2 receptor-nephrotic syndrome.
88 n natriuretic peptide], EDA2R [ectodysplasin A2 receptor], NPPB [B-type natriuretic peptide], BCAN [b
89 ine diminishes inflammation via occupancy of A2 receptors on inflammatory cells.
90 rcomeric DCM, including EDA2R (ectodysplasin A2 receptor; per log2 fold change in relative protein ab
91 rular basement membrane (GBM), phospholipase A2 receptor (PLA2R) and thrombospondin type 1 domain-con
92                            The phospholipase A2 receptor (PLA2R) and thrombospondin type-1 domain-con
93 d pretransplant levels of anti-phospholipase A2 receptor (PLA2R) antibodies were strongly associated
94 ard with the identification of phospholipase A2 receptor (PLA2R) as a target antigen in the majority
95          Identification of the phospholipase A2 receptor (PLA2R) as the major antigen in adults in 20
96    The characterization of the phospholipase A2 receptor (PLA2R) as the major target antigen in prima
97                The muscle-type phospholipase A2 receptor (PLA2R) has been identified as the principal
98                                Phospholipase A2 receptor (PLA2R) is a member of the mannose receptor
99                     The M-type phospholipase A2 receptor (PLA2R) is expressed in podocytes in human g
100                     The M-type phospholipase A2 receptor (PLA2R) is the major autoantigen of primary
101                      Secretory phospholipase A2 receptor (PLA2R) is the target antigen of the auto-an
102  was determined by ELISA using phospholipase A2 receptor (PLA2R) or Gd-IgA1 as antigen.
103 ht to determine the utility of phospholipase A2 receptor (PLA2R) staining for the detection of recurr
104 ranous nephropathy are against phospholipase A2 receptor (PLA2R), a cell surface receptor.
105                                Phospholipase A2 receptor (PLA2R)-associated membranous nephropathy (M
106 ve IgG4 autoantibodies against phospholipase A2 receptor (PLA2R).
107 ing IgG4 autoantibodies to the phospholipase A2 receptor (PLA2R).
108 oantibodies against the M-type phospholipase A2 receptor (PLA2R-AB) are a key biomarker in the diagno
109 ic variants in an HLA-DQA1 and phospholipase A2 receptor (PLA2R1) allele associate most significantly
110 oantibodies against the M-type phospholipase A2 receptor (PLA2R1) expressed on kidney podocytes, but
111                            The phospholipase A2 receptor (PLA2R1) is the major autoantigen in idiopat
112                            The phospholipase A2 receptor (PLA2R1) is the major autoantigen in primary
113 out the biological role of the phospholipase A2 receptor (PLA2R1) transmembrane protein.
114  the physiological role of the phospholipase A2 receptor (PLA2R1).
115               We examined the role adenosine A2 receptors play in the efficacy of neurotransmission b
116 45 min following the tetanus indicating that A2 receptors play no significant role in the maintenance
117           It has been shown in phospholipase A2 receptor positive membranous nephropathy that known a
118 racellular cAMP levels through activation of A2 receptors present on developing amacrine and ganglion
119 tion as the second intron of the thromboxane A2 receptor, prostaglandin D2 receptor, prostaglandin I2
120 -2-enoyl-coenzyme A reductase, phospholipase A2 receptor, protein kinase C zeta type, tubulin beta-4B
121 tor-beta binding protein 2 and ectodysplasin A2 receptor showed the strongest mediation across cohort
122 show that strengthening of the Ectodysplasin-A2-Receptor signalling axis in myogenic precursors and d
123 he effects of adenosine and adenosine Al and A2 receptor subtype agonists on in vitro perfused contro
124 ing the prognostic value of antiphospholipid A2 receptor, the risk of living-related donation, the li
125 creases Galphaq association with thromboxane A2 receptors thereby shifting them to a higher affinity
126 probably mediated by activation of adenosine A2 receptors through the PKC pathway, and (3) the preser
127 from astrocytes by a direct effect on A1 and A2 receptors, thus providing a link between actions of N
128           HHV-8 uses langerin and the ephrin A2 receptor to infect Langerhans cells, which support fu
129  vasodilatation, and stimulates carotid body A2 receptors to increase respiration.
130 eased by acute hypoxia stimulates A1 but not A2 receptors to produce muscle vasodilatation, and stimu
131  F2alpha receptor (FP) (61), and thromboxane A2 receptor (TP) (11) while sparing EP2, EP3, and prosta
132 he PGF2 alpha receptor (FP), the thromboxane A2 receptor (TP) and the prostacyclin receptor (IP).
133 lexibility of the purified human thromboxane A2 receptor (TP) was characterized by spectroscopic appr
134                            Human thromboxane A2 receptor (TP), a G protein-coupled receptor (GPCR), i
135 date the molecular mechanisms of thromboxane A2 receptor (TP)-induced insulin resistance in endotheli
136  Here, we show that vasopressive thromboxane A2 receptors (TP) can intimately couple with and inhibit
137       We explore here, using the thromboxane A2 receptor TPalpha, the ability of G12 and G13 to repor
138 tors; two splice variants of the thromboxane A2 receptor (TPalpha and TPbeta) have been cloned.
139 n of the signaling properties of thromboxane A2 receptor (TPalpha) -Galpha12 and -Galpha13 fusion con
140 g partner of the beta-isoform of thromboxane A2 receptor (TPbeta) by yeast two-hybrid screening.
141                                  Thromboxane A2 receptor (TPr) stimulation induces cellular hypertrop
142  oxidative stress, activates the thromboxane A2 receptor (TXAR) and the Rho-associated kinase (ROCK)
143 ing effect could be mediated by an adenosine A2 receptor via the protein kinase C (PKC) pathway.
144 elated, but distinct, X-linked ectodysplasin-A2 receptor (XEDAR).

 
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