ライフサイエンスコーパス: hyperresponsive

1 lation of 11% oxygen, and were classified as hyperresponsive.

2 to even a small extent (25% increase) become hyperresponsive.

3 leted and (2) Noe mice in which NK cells are hyperresponsive.

4 not exacerbate the developmental defects and hyperresponsive activity of A20-deficient B cells.

5 anded population of apoptosis-resistant, TLR-hyperresponsive alveolar macrophages that enhance airway

6 cted pronounced limbic volume reductions and hyperresponsive amygdala during emotional arousal, with

7 patitis, the monocytes of cHCV patients were hyperresponsive and failed to show homo- or heterotolera

8 l T and B cells, LAX(-/-) T and B cells were hyperresponsive and had enhanced calcium flux, protein t

9 ar dorsal horn multireceptive neurons became hyperresponsive and when behavioral nociceptive threshol

10 ar dorsal horn multireceptive neurons became hyperresponsive and when behavioral nociceptive threshol

11 f SLE is T cell dysfunction characterized by hyperresponsive antigen receptor signaling.

12 icient B cells, the E613R mutation generates hyperresponsive B cells.

13 h supraphysiologic CD45 expression exhibited hyperresponsive BCR signaling, they did so by opposite r

14 reased Btk association with the membrane and hyperresponsive BCR signaling.

15 These correspond with hyperresponsive calcium and pERK responses to TCR stimul

16 with fatal autoimmune-like disease caused by hyperresponsive CD4(+) T cells.

17 of a susceptible microenvironment can drive hyperresponsive CD45 E613R B cells to break tolerance.

18 B cells in the double mutant mice phenocopy hyperresponsive CD45 E613R B cells, whereas peripheral T

19 CTLA-4 knockout T cells are hyperresponsive compared with wild-type T cells in B7-fr

20 d increased adhesion on type I collagen, and hyperresponsive CRP and CLEC-2-induced alpha and dense g

21 This became apparent from the hyperresponsive degranulation of lyn-/- bone marrow-deri

22 as Jurkat T cells suppressed for IQGAP1 were hyperresponsive, displaying increased IL-2 and IFN-gamma

23 esponse to common life stressors, in which a hyperresponsive dopaminergic system is thought to play a

24 In the stress-hyperresponsive Fischer strain, P1-14 pups were isolated

25 gnificantly reduced SHP-1 activity, are also hyperresponsive following integrin engagement.

26 Itpkb(-/-) thymocytes are pre-TCR hyperresponsive, hyperactivate Akt, downstream mTOR and

27 A hyperresponsive immune system is suggested by the follic

28 ence indicating this system is overactive or hyperresponsive in depression and with genetic evidence

29 atory environment because the thymocytes are hyperresponsive in preinflammatory-stage Tgfb1(-/-) mice

30 ARAP3-deficient neutrophils are hyperresponsive in several adhesion-dependent situations

31 d that B cells lacking c-ets-1 are generally hyperresponsive in terms of Ab secretion and form large

32 The mutant B cells were not hyperresponsive in terms of proliferation and antibody p

33 Cells expressing active RhoA were thus hyperresponsive in the context of TCR-induced proliferat

34 avenously activates T cells, rendering cells hyperresponsive in vitro for at least two days after inj

35 mice that expressed CD1d only on thymocytes, hyperresponsive iNKT cells in the periphery expressed si

36 stricted expression of CD1d gives rise to Ag hyperresponsive iNKT cells.

37 sion developed a comparable population of Ag hyperresponsive iNKT cells.

38 nd whether the pathogenesis of IA involves a hyperresponsive mast cell compartment.

39 There was no evidence of a hyperresponsive mast cell phenotype in patients with IA.

40 Pep-deficient mice on the B6 background have hyperresponsive memory T cells, autoimmunity does not de

41 enia, and accumulation of a rapidly cycling, hyperresponsive memory-like CD8+CD44+ IL-7R- T cells whi

42 Wistar-Kyoto (WKY) rats exhibit hyperresponsive neuroendocrine and behavioral responses

43 beta1 is a novel marker of tissue homing and hyperresponsive neutrophil subtypes in sepsis, and block

44 ically results in hyporesponsive rather than hyperresponsive NK cells.

45 by either I/R or LPS and exhibited endotoxin hyperresponsive patterns (GCN5, CBP and p300).

46 Despite evidence of hyperresponsive peripheral and central nervous system (C

47 ls derived from Cyld knockout mice display a hyperresponsive phenotype and mediate the spontaneous de

48 Previous studies linked the hyperresponsive phenotype in part to increased Fyn kinas

49 ast, the P. aeruginosa pilA mutant induced a hyperresponsive phenotype in TLR2KO mice.

50 TNF-alpha in suspension, indicating that the hyperresponsive phenotype of the pir-b-/- cells during a

51 The hyperresponsive phenotype of TLR2KO mice exposed to the

52 Loss of Lyn resulted in a hyperresponsive phenotype on engagement of surface integ

53 o P-12LO-/- platelet-rich plasma rescues the hyperresponsive phenotype resulting in a diminished ADP-

54 three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from t

55 ly dependent on HY5 activity for their light-hyperresponsive phenotypes.

56 ng between various TLRs and NOD2 resulted in hyperresponsive, proinflammatory macrophages, thus provi

57 -) T cells, would exhibit an Ag-independent, hyperresponsive proliferation phenotype.

58 cells capable of suppressing AHR in the OVA-hyperresponsive recipients, but the process of sensitiza

59 ted in enhanced transcription, manifested by hyperresponsive recruitment of RNA polymerase II (Pol II

60 the Tnf-alpha gene, all exhibiting endotoxin hyperresponsive recruitment patterns similar to Pol II.

61 or SOCS1 and -3 in the seemingly paradoxical hyperresponsive state in cells deficient in IL-18Ralpha,

62 The hyperresponsive state that results leads to greatly magn

63 ives the paradoxical result of B cells being hyperresponsive, suggesting an inhibitory role for this

64 itory wedge motif in CD45 (E613R) results in hyperresponsive thymocytes and B cells on the C57BL/6 ba

65 B cells in Helios transgenic mice were also hyperresponsive to Ag stimulation.

66 Rasa3 mutant platelets were hyperresponsive to agonist stimulation, both in vitro an

67 ntal defects, T cells from these animals are hyperresponsive to anti-CD3 Ab stimulation.

68 er mononuclear cells from BTLA(-/-) mice are hyperresponsive to anti-CD3, Con A, and alpha-galactosyl

69 is not only aberrantly autoreactive but also hyperresponsive to antigen stimulation.

70 h these features, PEP-R619W lymphocytes were hyperresponsive to antigen-receptor engagement with a di

71 Cbl-b deficiency thus renders T cells hyperresponsive to antigenic stimulation and predisposes

72 of the WAS gene results in B cells that are hyperresponsive to B cell receptor and Toll-like recepto

73 verexpressing wild-type Btk were selectively hyperresponsive to BCR stimulation and showed enhanced C

74 Also, HBI1-overexpressing plants are hyperresponsive to BR and more resistant to the BR biosy

75 Seedlings with reduced BAS1 expression are hyperresponsive to brassinosteroids in a light-dependent

76 Bronchi from COX-1(-/-) mice were hyperresponsive to bronchoconstrictors.

77 AMP1/YP mice compared with control mice were hyperresponsive to CCL5 in chemotaxis.

78 Arabidopsis Isd1 mutants are hyperresponsive to cell death initiators and fail to lim

79 tic progenitor cells from SHIP(-/-) mice are hyperresponsive to certain hematopoietic growth factors,

80 rophils and DCs from pir-b-/- mice were also hyperresponsive to chemokine stimulation.

81 Nonetheless, these cells are hyperresponsive to cytokines and have characteristics of

82 lated conditions, these brain regions may be hyperresponsive to disease-specific emotional and affere

83 Antigen-challenged guinea pigs were hyperresponsive to electrical stimulation of the vagus n

84 ins-l flies are also hyperactive and hyperresponsive to environmental perturbations.

85 Accordingly, TCF1-deficient mice are hyperresponsive to experimental autoimmune encephalomyel

86 (BMMCs) from Lyn-deficient (Lyn-/-) mice are hyperresponsive to FcepsilonRI cross-linking with multiv

87 ped neutrophilia, and bone marrow cells were hyperresponsive to G-CSF stimulation.

88 PSGL-1(null) CD8(+) T cells were found to be hyperresponsive to homeostatic cytokines IL-2, IL-4, and

89 The mice are very hyperactive and hyperresponsive to human contact and other sensory stimu

90 lung, liver, and spleen iNKT cells that are hyperresponsive to hypoxia/reoxygenation.

91 sion rendered STAT3-deficient CD8(+) T cells hyperresponsive to IL-12, suggesting that the STAT3-SOCS

92 s expressed the high-affinity IL-2R and were hyperresponsive to IL-2.

93 indicates that p47(phox-/-) macrophages are hyperresponsive to IL-4 and show higher Stat6 phosphoryl

94 alternative activation and, furthermore, are hyperresponsive to IL-4 stimulation.

95 TSK/+ fibroblasts appeared to be hyperresponsive to IL-4, displaying increased synthesis

96 TFF2-/- cells were hyperresponsive to interleukin 1 beta stimulation but sh

97 hat is not secreted, thereby rendering cells hyperresponsive to interleukin-1beta stimulation.

98 entation groups designated shl for seedlings hyperresponsive to light.

99 teoclast progenitors from Nf1(+/-) mice were hyperresponsive to limiting concentrations of M-CSF and

100 MKP-1-/- mice are hyperresponsive to low-dose LPS-induced toxicity and exh

101 Furthermore, cells from Lcn2KO mice were hyperresponsive to LPS ex vivo, exhibiting elevated cyto

102 Moreover, LAB(-/-) mice were hyperresponsive to LPS-induced septic shock.

103 Naive ADAP-deficient CD8 T cells are hyperresponsive to lymphopenia in vivo and exhibit enhan

104 ks a regulator of G protein signaling and is hyperresponsive to mating pheromone.

105 A20-deficient B cells are hyperresponsive to multiple stimuli and display exaggera

106 or that OCL precursors in these lesions are hyperresponsive to osteoclastogenic factors (or both).

107 Furthermore, SA-deficient rice is hyperresponsive to oxidative damage caused by paraquat t

108 disease (XLP), who lack functional SAP, were hyperresponsive to PD-1 signaling, confirming its inhibi

109 at the absence of 4-1BB can make CD4 T cells hyperresponsive to protein Ag in vivo, suggesting a new

110 ursors derived from CYLD-deficient mice were hyperresponsive to RANKL-induced differentiation and pro

111 P392L)-transduced osteoclast precursors were hyperresponsive to receptor activator of NF-kappaB ligan

112 with a disrupted CD22 gene were found to be hyperresponsive to receptor signaling: Heightened calciu

113 CD4(+)CD8(+) and CD4(+)CD8(-) thymocytes are hyperresponsive to receptor-mediated and receptor-indepe

114 time that: i) mouse and human MAIT cells are hyperresponsive to SAgs, typified by staphylococcal ente

115 y to InsP3, which subsequently makes neurons hyperresponsive to stimulation and presumably more prone

116 LAX-deficient mast cells were hyperresponsive to stimulation via the Fc epsilonRI, as

117 cyte development, it caused mast cells to be hyperresponsive to stimulation via the FcepsilonRI, evid

118 CAM-1/Lyn double-deficient mice were equally hyperresponsive to stimulation with a GPVI-specific agon

119 ells from lupus-prone mice are intrinsically hyperresponsive to stimulation with antigen, particularl

120 CD4 T cells from ACS patients were also hyperresponsive to T cell receptor-mediated stimulation

121 The PTEN-deficient cells were also hyperresponsive to T-cell receptor (TCR) stimulation, as

122 Indeed, SAP-deficient T cells were hyperresponsive to T-cell receptor stimulation, which re

123 ligation of CD28; scurfy cells, however, are hyperresponsive to TCR ligation and exhibit a decreased

124 e we show that DGKzeta-deficient T cells are hyperresponsive to TCR stimulation both ex vivo and in v

125 G2A-deficient T cells are hyperresponsive to TCR stimulation, exhibiting enhanced

126 cells from mice lacking Sts-1 and Sts-2 are hyperresponsive to TCR stimulation.

127 In other experiments, D3R-/- mice were hyperresponsive to the administration of amylin and lept

128 is demonstrated that GP V -/- platelets were hyperresponsive to thrombin, resulting in increased fibr

129 studies identified that c-Cbl(-/-) HSCs are hyperresponsive to thrombopoietin (TPO) and display elev

130 BCAP-deficient macrophages and mice are hyperresponsive to TLR agonists and have reduced PI3K ac

131 egulators of immune activation and thus were hyperresponsive to TLR ligands, producing abnormally hig

132 on by small interference RNAs rendered cells hyperresponsive to TNF-alpha stimulation.

133 stituted with mutated p50 precursor p105 are hyperresponsive to TNFalpha stimulation relative to wild

134 Lyn-deficient DCs were hyperactivated and hyperresponsive to Toll-like receptor agonists and IL-1b

135 ver, infection of Ubp43(-/-) mice, which are hyperresponsive to type I IFNs, did not exhibit enhanced

136 ith posttraumatic stress disorder (PTSD) are hyperresponsive to unexpected or potentially threatening

137 Antigen-challenged animals were hyperresponsive to vagal stimulation, but those that rec

138 ECs infected by pathogenic hantaviruses are hyperresponsive to vascular endothelial growth factor (V

139 Mature coronary collateral arteries are hyperresponsive to vasopressin; in contrast, contractile

140 HO-2 deficiency caused hyperresponsive TRAM-dependent TLR4 signaling and hypers

141 Cbl-b double knock-out (dKO) T cells became hyperresponsive upon anti-CD3 stimulation, even though t

142 ath, even though the mice still maintained a hyperresponsive Vdr-deficient immune system.

143 nals) and mice overexpressing CD19 (that are hyperresponsive) were crossed with CD21- and C3-deficien