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1 ntly by lanthanum (IC50 = 2 microM) and were desensitized by 1 microM 2S,4R-4-methylglutamate (SYM 20
2    In contrast to the WT CXCR2, which is 93% desensitized by 20 nM ligand, the 331T, 342T, and 4A CXC
3 vo, EBI2-deficient B cells or normal B cells desensitized by 7alpha,25-OHC pre-treatment showed reduc
4  of immature thymocytes is not significantly desensitized by a negative concentration gradient of CKb
5 eptor is exposed to bright light, the rod is desensitized by a process known as bleaching adaptation.
6 ntrast, GABA(B)R-mediated GIRK currents were desensitized by a similar amount after only 2 h of agoni
7  majority of G protein-coupled receptors are desensitized by a uniform two-step mechanism: phosphoryl
8 (baclofen) treatment for up to 48 h, and was desensitized by about one-half after 96 h.
9                     Both CXCR4 and CCR5 were desensitized by activation of the cells with WKYMVm via
10  while a second class could be activated and desensitized by Ala, Cys, Glu, or Gly.
11 A-induced Ca(2+) flux in monocytes was cross-desensitized by an agonistic ligand MMK-1 specific for f
12  mobilization in monocytes can also be cross-desensitized by an FPRL1-specific agonist.
13         A third class could be activated and desensitized by any of the six effective amino acids.
14 a(2+)channel coupling in dorsal root ganglia desensitized by ARM390 and the rate of resensitization w
15 ed by pertussis toxin and suramin and can be desensitized by ATP and ADP, suggesting a P2Y type nucle
16 eptor-selective antagonist and was not cross-desensitized by ATP.
17                                    For cells desensitized by bleaching, light adaptation of both comp
18 adapted, and show that, for rods permanently desensitized by bleaching, the desensitization is not du
19 R), CXCR2 was cross-phosphorylated and cross-desensitized by C5a and fMLP.
20 protein signaling is rapidly terminated (or "desensitized") by calcium influx through voltage-gated c
21 mn at the lumbar 2 (L2) segments, which were desensitized by capsaicin.
22 ecently found to be both fully activated and desensitized by choline, in addition to ACh.
23 icantly greater than in A7 cells and was not desensitized by chronic morphine.
24 gger deletion, however, when the BCRs become desensitized by chronic stimulation with self-antigens o
25  endothelial transmigration of Th1 cells was desensitized by CXCL9.
26 lization by S3 and DeltaCCR1 were also cross-desensitized by CXCR1 and CXCR2 despite lack of receptor
27 5aR nor FR was cross-phosphorylated or cross-desensitized by CXCR2 activation, although CXCR1 did med
28                                         MORs desensitized by DAMGO activation are then readily intern
29 tor neurons in male antennae were completely desensitized by direct application of metyrapone into th
30 was lower than that for CCR9B, and CCR9A was desensitized by doses of CCL25 that failed to silence CC
31                       Intact LH/CG R was not desensitized by ectopic arrestin3 constructs.
32  A, like DeltaST, could not be significantly desensitized by exposure to agonist, mutant B exhibited
33   These results suggest that NK cells may be desensitized by exposure to NKG2D ligands.
34                     The ASICs were gated and desensitized by extracellular application of millimolar
35 , indicating that the channels are partially desensitized by extracellular nucleotides.
36 d by PAF, and cross-phosphorylated and cross-desensitized by fMet-Leu-Phe, C5a, and IL-8.
37 bers of this receptor family are regulated ("desensitized") by G protein-coupled receptor kinase (GRK
38             In simple model systems, CB1R is desensitized by GRK phosphorylation at two serine residu
39    AdipoR1 is phosphorylatively modified and desensitized by GRK2 in failing cardiomyocytes, contribu
40                   Here we show that TRPA1 is desensitized by homologous (mustard oil; a TRPA1 agonist
41 g hypoglycaemia when the carotid bodies were desensitized by hyperoxia.
42                Basophils in whole blood were desensitized by incubation with twofold to 2.5-fold incr
43 responsible for their beneficial actions are desensitized by infection.
44 R2-specific calcium flux and chemotaxis were desensitized by injury, returning toward normal after 1
45 ization is dependent on arrestins and can be desensitized by long-term exposure to an agonist.
46          These data indicate hepatocytes are desensitized by LPS in a TLR4 signaling-dependent manner
47  CRAMP-induced calcium flux in monocytes was desensitized by MMK-1, an agonistic ligand specific for
48  arrestin-dependent mechanism, whereas those desensitized by morphine are not.
49 he alpha5 subunit are potently activated and desensitized by nanomolar concentrations of nicotine.
50  current in the VTA/SNc is not significantly desensitized by nicotine in the range < or =100 nm.
51 AMP response, whereas the mutant receptor is desensitized by only approximately 20%.
52 ediates prolonged signaling and is not cross-desensitized by OnM.
53 om rat tail artery and vas deferens are also desensitized by OXY, but not by NE or PE, indicating tha
54     PAFR was homologously phosphorylated and desensitized by PAF, and cross-phosphorylated and cross-
55  were neither cross-phosphorylated nor cross-desensitized by PAF.
56 entration in response to Alternaria that was desensitized by peptide and protease ligands for PAR-2 a
57 ranulation was pertussis toxin sensitive and desensitized by preincubating cells with G protein-coupl
58 aggregation response to LPA was specifically desensitized by prior addition of Sph-1-P.
59  induced a Ca2+ flux in THP-1 cells that was desensitized by prior exposure to RANTES.
60 rowth-related oncogene alpha (Groalpha), was desensitized by prior exposure to the chemoattractants N
61 SDF-1 in DeltaCyto CXCR4 cells was partially desensitized by prior treatment with SDF-1.
62 ecovers the agonist sensitivity of receptors desensitized by prolonged exposure to capsaicin.
63 Ca(2+) mobilization, and were only partially desensitized by RANTES, relative to S1 and CCR1.
64        Histamine increase in [Ca(2+)](i) was desensitized by repeated addition of agonist and blocked
65 so induced calcium mobilization that was not desensitized by repeated additions.
66                                     B(2) was desensitized by repeated administration of BK but resens
67                                However, skin desensitized by repeated capsaicin application showed no
68                       The depolarization was desensitized by repeated exposure to factors and was not
69 H1R-mediated adenylyl cyclase responses were desensitized by repetitive PTH challenges in a concentra
70  mobilization in lymphocytes, which could be desensitized by SDF-1, suggesting possible cross-regulat
71 dermal growth factor receptor (EGFR), may be desensitized by serine/threonine kinases.
72 ed alpha7-mediated nicotinic EPSCs also were desensitized by superfusion with 1 microM nicotine, had
73 , yet nearly all affected individuals can be desensitized by the administration of graded doses of as
74 ly restored the response of the B2 receptor, desensitized by the agonist (1 mumol/L [Hyp3-Tyr(Me)8]BK
75  Ca2+ entry as the response to capsaicin was desensitized by the same amount whether prior exposure t
76 erization in eosinophils and neutrophils was desensitized by the same combinations of chemoattractant
77        BL activation of pump current becomes desensitized by three or four pulses of 30 s x 100 micro
78 n release of glutamate, synaptic AMPARs were desensitized by transmitter by >90%.
79 ugh Flag-hkorS358N was not phosphorylated or desensitized by (-)U50,488H stimulation, Flag-rkorN358S
80                  The nSTR, pSTR and pSR were desensitized by weaker backgrounds than those desensitiz

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