ライフサイエンスコーパス: desensitized by

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 rom the plasma membrane and are subsequently desensitized by beta-arrestin (beta-arr).

18 Stimulated GLP-1Rs are rapidly desensitized by beta-arrestins, scaffolding proteins tha

19 For cells desensitized by bleaching, light adaptation of both comp

20 adapted, and show that, for rods permanently desensitized by bleaching, the desensitization is not du

21 R), CXCR2 was cross-phosphorylated and cross-desensitized by C5a and fMLP.

22 protein signaling is rapidly terminated (or "desensitized") by calcium influx through voltage-gated c

23 mn at the lumbar 2 (L2) segments, which were desensitized by capsaicin.

24 ecently found to be both fully activated and desensitized by choline, in addition to ACh.

25 icantly greater than in A7 cells and was not desensitized by chronic morphine.

26 gger deletion, however, when the BCRs become desensitized by chronic stimulation with self-antigens o

27 endothelial transmigration of Th1 cells was desensitized by CXCL9.

28 lization by S3 and DeltaCCR1 were also cross-desensitized by CXCR1 and CXCR2 despite lack of receptor

29 5aR nor FR was cross-phosphorylated or cross-desensitized by CXCR2 activation, although CXCR1 did med

30 MORs desensitized by DAMGO activation are then readily intern

31 tor neurons in male antennae were completely desensitized by direct application of metyrapone into th

32 was lower than that for CCR9B, and CCR9A was desensitized by doses of CCL25 that failed to silence CC

33 Intact LH/CG R was not desensitized by ectopic arrestin3 constructs.

34 ensitivity curves that show a hair bundle is desensitized by efferent stimulation.

35 A, like DeltaST, could not be significantly desensitized by exposure to agonist, mutant B exhibited

36 These results suggest that NK cells may be desensitized by exposure to NKG2D ligands.

37 The ASICs were gated and desensitized by extracellular application of millimolar

38 , indicating that the channels are partially desensitized by extracellular nucleotides.

39 d by PAF, and cross-phosphorylated and cross-desensitized by fMet-Leu-Phe, C5a, and IL-8.

40 bers of this receptor family are regulated ("desensitized") by G protein-coupled receptor kinase (GRK

41 In simple model systems, CB1R is desensitized by GRK phosphorylation at two serine residu

42 AdipoR1 is phosphorylatively modified and desensitized by GRK2 in failing cardiomyocytes, contribu

43 Here we show that TRPA1 is desensitized by homologous (mustard oil; a TRPA1 agonist

44 g hypoglycaemia when the carotid bodies were desensitized by hyperoxia.

45 Basophils in whole blood were desensitized by incubation with twofold to 2.5-fold incr

46 responsible for their beneficial actions are desensitized by infection.

47 R2-specific calcium flux and chemotaxis were desensitized by injury, returning toward normal after 1

48 ization is dependent on arrestins and can be desensitized by long-term exposure to an agonist.

49 These data indicate hepatocytes are desensitized by LPS in a TLR4 signaling-dependent manner

50 CRAMP-induced calcium flux in monocytes was desensitized by MMK-1, an agonistic ligand specific for

51 arrestin-dependent mechanism, whereas those desensitized by morphine are not.

52 he alpha5 subunit are potently activated and desensitized by nanomolar concentrations of nicotine.

53 current in the VTA/SNc is not significantly desensitized by nicotine in the range < or =100 nm.

54 AMP response, whereas the mutant receptor is desensitized by only approximately 20%.

55 ediates prolonged signaling and is not cross-desensitized by OnM.

56 om rat tail artery and vas deferens are also desensitized by OXY, but not by NE or PE, indicating tha

57 PAFR was homologously phosphorylated and desensitized by PAF, and cross-phosphorylated and cross-

58 were neither cross-phosphorylated nor cross-desensitized by PAF.

59 entration in response to Alternaria that was desensitized by peptide and protease ligands for PAR-2 a

60 ls lacking the mitochondrial ATP synthase is desensitized by pharmacological inhibition and genetic d

61 Neurons were desensitized by pre-exposing flies to the odorant, but t

62 ranulation was pertussis toxin sensitive and desensitized by preincubating cells with G protein-coupl

63 aggregation response to LPA was specifically desensitized by prior addition of Sph-1-P.

64 induced a Ca2+ flux in THP-1 cells that was desensitized by prior exposure to RANTES.

65 rowth-related oncogene alpha (Groalpha), was desensitized by prior exposure to the chemoattractants N

66 SDF-1 in DeltaCyto CXCR4 cells was partially desensitized by prior treatment with SDF-1.

67 ecovers the agonist sensitivity of receptors desensitized by prolonged exposure to capsaicin.

68 Ca(2+) mobilization, and were only partially desensitized by RANTES, relative to S1 and CCR1.

69 Histamine increase in [Ca(2+)](i) was desensitized by repeated addition of agonist and blocked

70 so induced calcium mobilization that was not desensitized by repeated additions.

71 B(2) was desensitized by repeated administration of BK but resens

72 However, skin desensitized by repeated capsaicin application showed no

73 The depolarization was desensitized by repeated exposure to factors and was not

74 H1R-mediated adenylyl cyclase responses were desensitized by repetitive PTH challenges in a concentra

75 mobilization in lymphocytes, which could be desensitized by SDF-1, suggesting possible cross-regulat

76 dermal growth factor receptor (EGFR), may be desensitized by serine/threonine kinases.

77 ed alpha7-mediated nicotinic EPSCs also were desensitized by superfusion with 1 microM nicotine, had

78 , yet nearly all affected individuals can be desensitized by the administration of graded doses of as

79 ly restored the response of the B2 receptor, desensitized by the agonist (1 mumol/L [Hyp3-Tyr(Me)8]BK

80 nd alpha2-containing receptors were potently desensitized by the epibatidine analogs.

81 Ca2+ entry as the response to capsaicin was desensitized by the same amount whether prior exposure t

82 erization in eosinophils and neutrophils was desensitized by the same combinations of chemoattractant

83 BL activation of pump current becomes desensitized by three or four pulses of 30 s x 100 micro

84 n release of glutamate, synaptic AMPARs were desensitized by transmitter by >90%.

85 ugh Flag-hkorS358N was not phosphorylated or desensitized by (-)U50,488H stimulation, Flag-rkorN358S

86 The nSTR, pSTR and pSR were desensitized by weaker backgrounds than those desensitiz