ライフサイエンスコーパス: ligand stimulation

1 nuclear Smad3 was a more precise outcome of ligand stimulation.

2 ted in dissociated sympathetic neurons after ligand stimulation.

3 lated on tyrosine residues in the absence of ligand stimulation.

4 tle colocalization was observed after 4 h of ligand stimulation.

5 NF receptor-associated factor 2 (TRAF2) upon ligand stimulation.

6 h components of the ERK1/2 cascade following ligand stimulation.

7 cAMP response and Erk phosphorylation after ligand stimulation.

8 stitutive complexes that are not affected by ligand stimulation.

9 ty to produce IL-12p70 after subsequent CD40 ligand stimulation.

10 recruited to TLR2 signalling complexes after ligand stimulation.

11 a (TGF-beta) receptors are internalized upon ligand stimulation.

12 m endogenous arachidonic acid in response to ligand stimulation.

13 ce of ephrin-A ligands and is disrupted upon ligand stimulation.

14 ne proteins translocate to the nucleus after ligand stimulation.

15 ptors and translocated into the nucleus upon ligand stimulation.

16 blot analysis and immunoprecipitation after ligand stimulation.

17 and recruited to the CD40 receptor upon CD40 ligand stimulation.

18 pathways can be conditionally activated upon ligand stimulation.

19 th the C-terminal Src kinase (CSK) following ligand stimulation.

20 ated with Stat1 but not Stat2 or Stat3 after ligand stimulation.

21 ors of transcription 5 (STAT5) activation on ligand stimulation.

22 that initiate signal cascades in response to ligand stimulation.

23 e activated in normal neurons in response to ligand stimulation.

24 tional mode of signal transduction following ligand stimulation.

25 as variable responsiveness to exogenous Wnt ligand stimulation.

26 amily receptor signaling in conjunction with ligand stimulation.

27 ion of type I IFNs and IL12p40 following TLR ligand stimulation.

28 enhanced activation of EGFR signalling upon ligand stimulation.

29 and independent of adaptation to persistent ligand stimulation.

30 ownstream cytokine expression in response to ligand stimulation.

31 re defective in cytokine production upon RLR ligand stimulation.

32 ore than doubled the sensitivity of cells to ligand stimulation.

33 phorylated, ubiquitinated, and degraded upon ligand stimulation.

34 somes and lysosome-mediated degradation upon ligand stimulation.

35 elective and undergoes dynamic regulation by ligand stimulation.

36 the activation of T cells via specific notch ligand stimulation.

37 and degraded in the lysosome upon long-term ligand stimulation.

38 d degradation of the receptor in response to ligand stimulation.

39 erleukin-8 and MCP-1 in response to specific ligand stimulation.

40 d intranuclear mobility especially following ligand stimulation.

41 localization, and reduced responsiveness to ligand stimulation.

42 ivation events in response to membrane-bound ligand stimulation.

43 th an activated TGFbeta receptor and TGFbeta ligand stimulation.

44 ignal-regulated kinase ERK1 and -2 following ligand stimulation.

45 esses and inhibits the activity of MAPK upon ligand stimulation.

46 eceptor Smoothened in the primary cilia upon ligand stimulation.

47 ed protein kinase activation is sustained on ligand stimulation.

48 lation in response to constant extracellular ligand stimulation.

49 otch1 in presence of myocardin or by Jagged1 ligand stimulation.

50 e promote their rapid interactions only upon ligand stimulation.

51 recruited independently to IL-1R1 following ligand stimulation.

52 to induce Erk phosphorylation in response to ligand stimulation.

53 epidermal growth factor or heregulin (a HER3 ligand) stimulation.

54 mplexes of Lyn-Cbl and Cbl-p85 exist without ligand stimulation, (2) upon ligand binding, Lyn becomes

55 R) can lead to cell transformation, and with ligand stimulation, a broader spectrum of phosphorylated

56 Upon ligand stimulation, a fragment of Notch is released prot

57 pathway activity specifically in response to ligand stimulation--a process that involves endocytic tr

58 re transcription sites, indicating that upon ligand stimulation, AhR is recruited to active transcrip

59 accumulate at or are depleted from points of ligand stimulation along the axons.

60 ion by desensitizing Met signaling following ligand stimulation and by eliminating potentially oncoge

61 ithin an embryonic epithelial sheet by local ligand stimulation and coordinates a long-range contract

62 l maturation of LSECs can be achieved by TLR ligand stimulation and elucidated the mechanisms involve

63 sought to characterize pathway targets using ligand stimulation and genetic models of activation.

64 Also, severe oxidative stress (unlike ligand stimulation and moderate oxidative stress, both o

65 orms, with PKCtheta being more responsive to ligand stimulation and PKCalpha/beta to growth-factor av

66 maturation exclusively in response to TLR1/2 ligand stimulation and that the immunological status of

67 ncreasing ESR1 protein cellular content upon ligand stimulation and upregulated the expression of est

68 -derived growth factor (PDGF) receptor after ligand stimulation, and binding of SHPTP2 to this recept

69 ate microtiter plates, one for cell culture, ligand stimulation, and cell lysis/receptor solubilizati

70 and dephosphorylated receptor in response to ligand stimulation, and that this may be a general mecha

71 In response to membrane-bound ligand stimulation, antigen aggregation occurs in B cell

72 After ligand stimulation, approximately 60-70% of transfected

73 e plasma membrane and is overactivated after ligand stimulation because of destabilization and degrad

74 growth, and slow their cell cycle following ligand stimulation but show increased cellular migration

75 creases in effector activity after 15 min of ligand stimulation, but only the serine phosphorylation

76 diated innate immunity due to inadequate Wnt ligand stimulation by monocytes provides an additional m

77 ution of the AhR/ARNT complex in response to ligand stimulation, by using live-cell confocal and high

78 which rapidly attenuate signals elicited by ligand stimulation, causing desensitization.

79 At low levels of receptor and UCP2, ligand stimulation creates a distinct temporal response

80 Upon ligand stimulation, epidermal growth factor receptor (EG

81 After PPARgamma ligand stimulation, HMGA1 and PPARgamma were recruited t

82 ative stability of IGF-IR in the presence of ligand stimulation, IGF-IR ubiquitination sites have yet

83 This mutant receptor fails to respond to ligand stimulation, implicating the GREAT gene in the et

84 f the HERP family, HERP1, was not induced by ligand stimulation in any cells tested, leading to the s

85 dings indicate that EGFR does not respond to ligand stimulation in M phase and suggest that a negativ

86 g, conditional deletion, mosaic analysis and ligand stimulation in mice to determine that both villou

87 e studies suggest a role for continuous self-ligand stimulation in the periphery for the maintenance

88 s were hyper-responsive to anti-IgM and TLR7 ligand stimulation in vitro and produced high concentrat

89 he ALK1 pathway and respond robustly to ALK1 ligand stimulation in vitro.

90 be up-regulated by chemokine CXCL13 and CD40 ligand stimulation in wild-type B cells, elevation of ly

91 Rgamma, increased activation was observed by ligand stimulation, indicating that both PPARgamma-depen

92 Ligand stimulation induced phosphorylation of cortactin

93 oughout receptor internalization, direct EGF ligand stimulation initiates the internalization of EGFR

94 - and hetero-oligomers both before and after ligand stimulation is controversial.

95 oop may contribute to the mechanism by which ligand stimulation is coupled to discrete biological res

96 way by which arachidonate released following ligand stimulation is made available only to prostagland

97 at tonic T cell receptor signaling from self-ligand stimulation is required to maintain a basal state

98 let-derived growth factor receptor ECD, upon ligand stimulation, is coupled to its intracellular doma

99 with lipid rafts in the apparent absence of ligand stimulation, it has been proposed that raft-assoc

100 Our results provide evidence that ligand stimulation leads to internalization of the insul

101 t was less responsive to H3 relaxin based on ligand stimulation of cAMP production.

102 Data herein show that ligand stimulation of cells that express both the EGFR a

103 In contrast, CD95 ligand stimulation of cells unable to internalize CD95 r

104 ponses to provocative stimulation, including ligand stimulation of cultured cardiomyocytes, pressure

105 1R) inhibitors had a synergistic effect, and ligand stimulation of EGFR and MET rescued DDR2-mutant l

106 Herein, we demonstrate that ligand stimulation of EphA2 promotes the nucleus translo

107 The results show that ligand stimulation of Flt3 can induce association of SOC

108 Ligand stimulation of fTie1 resulted in Tie1 autophospho

109 f Cl- flux reflected selective disruption of ligand stimulation of GCC rather than the chloride chann

110 taurosporine treatment of HeLa cells and Fas ligand stimulation of Jurkat cells.

111 ucts is not reduced by DEP or PAHs following ligand stimulation of macrophages or fibroblasts.

112 It is also well established that ligand stimulation of many plasma membrane receptors lea

113 Instead, ligand stimulation of mGluR5 caused a dynamic transactiv

114 By contrast, ligand stimulation of non-overexpressed ERBB2 transientl

115 e mechanism of signal transmission following ligand stimulation of receptor tyrosine kinases in livin

116 These observations indicate that ligand stimulation of RTKs is not generic, and point to

117 xpressing RAGEv1 in tumor cells altered RAGE ligand stimulation of several novel classes of genes tha

118 in 293T and NIH 3T3 cells demonstrated that ligand stimulation of several RPTKs (epidermal growth fa

119 tic cell, G proteins in the Gq family couple ligand stimulation of the m1 muscarinic receptor to acti

120 timulates a similar Ca2+ transient as native ligand stimulation of the naive precursors, consistent w

121 Upon ligand stimulation of the receptors, Jaks are activated

122 Moreover, altered peptide ligand stimulation of the Th1 line stimulates a similar

123 In particular, ephrin-A ligand stimulation of tumor cells induces EphA2 receptor

124 ivation of signaling pathways in response to ligand stimulation of upstream cell surface receptors.

125 stimulation of Eph-B4 signaling, either via ligand stimulation or expression of a constitutively act

126 ibited genotype selection under RTK-targeted ligand stimulation or pharmacologic inhibition in vitro.

127 or ATPgammaS effectively sensitized GC-A to ligand stimulation over prolonged periods of time in eit

128 On EGFR ligand stimulation, phosphorylation of PLCgamma-1 increa

129 Following ligand stimulation, phosphorylation of specific tyrosyl

130 Ligand stimulation promoted recruitment of PELP1 to 17be

131 Furthermore, the mutated receptor was, upon ligand-stimulation, quickly internalized and degraded.

132 d cytokine responses to TLR4 ligand and TLR5 ligand stimulation relative to PB DCs, yet similarly pro

133 MP2A induces a heightened sensitivity to TLR ligand stimulation, resulting in increased proliferation

134 Receptor activator for NF-kappaB (RANK) ligand stimulation results in IFN-beta upregulation, whi

135 A proteolytic cascade induced by ligand stimulation results in release of the intracellul

136 Activation of FGFR3, through mutation or ligand stimulation, results in autophosphorylation of mu

137 After Fas ligand stimulation, SB-HCV-infected Molt-4 cells had inc

138 Upon ER Ca(2+) depletion or via ligand stimulation, Sig-1Rs dissociate from BiP, leading

139 to produce large amounts of IL-12 after CD40 ligand stimulation, similar to IL-4 priming of DCs.

140 (InsP3R) channels responding to incremental ligand stimulation, single-channel patch-clamp electroph

141 t down-regulation efficiently in response to ligand stimulation, suggesting that activation of classi

142 ntly delays dephosphorylation of CXCR2 after ligand stimulation, suggesting that clathrin-mediated en

143 Upon ligand stimulation, TGFbeta receptors phosphorylate Smad

144 with the IGF-I receptor (IGF-IR), and after ligand stimulation the association of IGF-IR with Galpha

145 After ligand stimulation, the internalized CXCR2 colocalized w

146 In this report, we demonstrate that, after ligand stimulation, the PDGF beta receptor (PDGFRbeta) b

147 In contrast, with TLR2 ligand stimulation, TNF-alpha production was reduced, wh

148 addition to receptor activator of NF-kappaB ligand stimulation to initiate greater bone remodeling.

149 phosphorylation in response to non-androgen ligand stimulation using phospho-specific antibodies.

150 ar cytokine production in the absence of TLR ligand stimulation was elevated in cells from older comp

151 The initial response to ligand stimulation was increased and sensitization to re

152 okine production in mast cells following TLR ligand stimulation was markedly reduced by HIF-1alpha kn

153 e the cell populations able to respond to Hh ligand stimulation, we expressed an oncogenic allele of

154 tor (IR)/IGF-1R is augmented upon respective ligand stimulation, whereas association with STAT3 is co

155 pithelial alphaTN4-1 cells in the absence of ligand stimulation, whereas the mutants exhibited signif

156 nderwent rapid cellular internalization upon ligand stimulation, whereas the TRAIL/DR4 complex was no

157 The effects can be reversed by ligand stimulation, which triggers the intrinsic tumor s

158 On ligand stimulation with CB agonists, CB receptors induce

159 Ligand stimulation with Sema6A does not change the degre