ライフサイエンスコーパス: transcription factor AP-1

1 c-Jun forms as a heterodimer with c-Fos, the transcription factor AP-1.

2 ascade, which is essential for activation of transcription factor AP-1.

3 ity, increased c-fos and c-jun mRNAs and the transcription factor AP-1.

4 nthesis-through the oxidative stress related transcription factor AP-1.

5 olving the opioid-mediated activation of the transcription factor AP-1.

6 and the reporter activity of the downstream transcription factor AP-1.

7 ed by estrogen in a process dependent on the transcription factor AP-1.

8 cade involving jun N-terminal kinase and the transcription factor AP-1.

9 of interleukin (IL)-8 via activation of the transcription factor AP-1.

10 diated via the JNK signaling pathway and the transcription factor AP-1.

11 f TREM-1 in mouse macrophages partly via the transcription factor AP-1.

12 monstrated that Lys-des-Arg-BK activates the transcription factor AP-1.

13 zipper) with Jun family members to form the transcription factor AP-1.

14 ansducin and accompanied by induction of the transcription factor AP-1.

15 levels and suppression of activation of the transcription factor AP-1.

16 un and Nrf2, two components of the oncogenic transcription factor AP-1.

17 functions as a subunit of the heterodimeric transcription factor AP-1.

18 phatidylcholine hydrolysis and activates the transcription factor AP-1.

19 and stimulation of transcription mediated by transcription factor AP-1.

20 ect on activation of another redox-sensitive transcription factor, AP-1.

21 N-terminal kinase, and of the Jun-containing transcription factor AP-1, a regulator of cellular stres

22 regulation of the best known immediate early transcription factor, AP-1; a heterodimer of the basic l

23 ho were involved in the shear stress-induced transcription factor AP-1 acting on the 12-O-tetradecano

24 Activation of the transcription factor AP-1 (activator protein-1) is requi

25 iated suppression of another CCL2-regulating transcription factor, AP-1 (activator protein-1).

26 Transcription factor AP-1 and alpha2beta1 integrin, whic

27 eptors includes up-regulation of the nuclear transcription factor AP-1 and AP-1 transcriptional activ

28 Lead activated the transcription factor AP-1 and increased AP-1-dependent l

29 cJun is a major component of the transcription factor AP-1 and mediates a diverse set of

30 aling pathways such as the activation of the transcription factor AP-1 and modulation of Wnt signalin

31 through an IL-11-dependent pathway involving transcription factor AP-1 and STAT3.

32 ) was down-regulation of the activity of the transcription factor AP-1 and subsequent coordinate redu

33 ephosphorylation of the c-Fos subunit of the transcription factor AP-1 and thereby inhibited TLR4-tri

34 G) ratios, and activation of stress-response transcription factors (AP-1 and NF-kappaB) were measured

35 el to DNA nucleated the concerted binding of transcription factors AP-1 and C/EBP beta to the 5'-regu

36 ces matching the consensus binding sites for transcription factors AP-1 and C/EBP.

37 Within minutes, low-dose UVB upregulated the transcription factors AP-1 and NF-kappa B, which are kno

38 antly inhibits both DA-induced activation of transcription factors AP-1 and NF-kappaB and subsequent

39 vents in the cell nucleus, the activation of transcription factors AP-1 and NF-kappaB by ultraviolet

40 The redox-sensitive transcription factors AP-1 and NF-kappaB have been impli

41 /TIMP-1 RNA abundance with activation of the transcription factors AP-1 and NF-kappaB in the lungs of

42 tumor necrosis factor (TNF-alpha) stimulate transcription factors AP-1 and NF-kappaB through activat

43 DNA binding of transcription factors AP-1 and NF-kappaB was not affecte

44 The signaling events activate the transcription factors AP-1 and NF-kappaB, leading to the

45 es such as c-jun and c-fos and activates the transcription factors AP-1 and NF-kappaB.

46 stitutive activation of the immunoregulatory transcription factors AP-1 and NF-kappaB.

47 optosis in vivo is mediated by activation of transcription factors AP-1 and NF-kappaB.

48 ctivation of c-Jun N-terminal kinase and the transcription factors AP-1 and NFAT but does not affect

49 emic area showed enhanced DNA binding of the transcription factors AP-1 and nuclear factor (NF)-kappa

50 we examine the role of the redox-responsive transcription factors AP-1 and nuclear factor-kappaB (NF

51 TNF-alpha messenger RNA (mRNA) levels and transcription factors AP-1 and nuclear factor-kappaB (NF

52 y we determined that inflammation responsive transcription factors AP-1 and SAF-1 synergistically reg

53 pounds that blocks the activation of two key transcription factors, AP-1 and NF-kappa B.

54 The transcription factors, AP-1 and nuclear factor kappaB (N

55 o found that NAC increased two IL-4 relevant transcription factors (AP-1) and NFATc.

56 of transcription, does not affect binding of transcription factor AP-1, and appears to involve a mech

57 tionally regulated by UV irradiation through transcription factor AP-1, and mediates altered collagen

58 ression through an AP-1 site and its cognate transcription factor AP-1, and requires the involvement

59 nts, inhibited the TNF-induced activation of transcription factor AP-1, and suppressed the TNF-induce

60 ivity, inhibition of DNA binding activity of transcription factor AP-1, and suppression of in vivo tr

61 al transduction, growth factors activate the transcription factor AP-1, and we show that this in turn

62 hat FGF-2 stimulates DNA binding activity of transcription factor AP-1 but not NF-kappaB and that AP-

63 ated protein kinase (MAP kinase) pathway and transcription factors (AP-1), but are toxic at high conc

64 ade specifically inhibited activation of the transcription factor AP-1 by TGF-beta1, whereas PD98059

65 lso suppressed TNF-induced activation of the transcription factor AP-1, c-jun N-terminal kinase and M

66 xhibit decreased DNA binding activity of the transcription factor, AP-1, compared with monocytes.

67 T(reg) cells downregulated expression of the transcription factor AP-1 complex and suppressed other T

68 The transcription factor AP-1, composed of Fos-Jun dimers, m

69 uch as Pin1 and Men1, that regulate the host transcription factor AP-1 controlling host inflammation,

70 regulated kinase, and p38, and activation of transcription factors AP-1, CREB, NF-kappaB, and STAT1 a

71 vated the binding of three oxidant-sensitive transcription factors: AP-1, CREB, and nuclear respirato

72 c-jun protein expression, and an increase in transcription factor AP-1 DNA binding activity.

73 were peripheral myelin protein 22, decorin, transcription factor AP-1, dystroglycan 1, myelin protei

74 clase Rutabaga, the Ig-CAM Fasciclin II, the transcription factor AP-1 (Fos/Jun), and the adhesion pr

75 ombin-induced CD44 expression is mediated by transcription factor AP-1 in a NADPH oxidase-dependent m

76 17C expression through the activation of the transcription factor AP-1 in a p38 MAPK-dependent manner

77 irradiation is mediated via induction of the transcription factor AP-1 in human skin fibroblasts.

78 nscription and mobilization of the mitogenic transcription factor, AP-1, in response to DOR1 signalin

79 n and functional assays, have implicated the transcription factor, AP-1, in the regulation of program

80 Although down regulation of the transcription factor AP-1 is highly prevalent in leiomyo

81 Because the transcription factor AP-1 is important for tumor promote

82 Transcription factor AP-1 is known to make specific cont

83 e transcriptional level, and that binding of transcription factor AP-1 is not affected.

84 In contrast, the transcription factor AP-1 is not required for activation

85 hat tumor promoter induced activation of the transcription factor AP-1 is required for induced neopla

86 iously reported that a JunD homodimer of the transcription factor AP-1 is specifically activated by T

87 As a transcription factor, AP-1 is commonly found as a hetero

88 The ubiquitous family of dimeric transcription factors AP-1 is made up of Fos and Jun fam

89 on the integrity of NF-E2 recognition sites, transcription factor AP-1-like protein-binding motifs, l

90 on at the IFNB1 promoter through activity at transcription factor AP-1-like sites.

91 P) kinase pathway and the binding of nuclear transcription factors (AP-1, NF-kappaB, and C/EBP) and s

92 Consensus binding sequences for the transcription factors AP-1, NF-kappaB and Sp1 were modif

93 ssion of the activity of the proinflammatory transcription factors AP-1, NF-kappaB, and STAT1.

94 overexpression of Fra-1, a component of the transcription factor AP-1, offers prognostic potential.

95 omplex formed between NFAT and the mitogenic transcription factor AP-1 on the interleukin-2 enhancer.

96 racellular signal-regulated kinase), and the transcription factors AP-1 or NF-kappaB.

97 and vitamin D-metabolic pathways via early- (transcription factor AP-1-related) and late-phase (initi

98 We demonstrate that HCV-induced transcription factors AP-1, Sp1, NF-kappaB and STAT-3 ar

99 n part by antagonizing the activities of the transcription factors AP-1, STAT and NF-kappaB.

100 exclude the inhibitory effect and shown that transcription factors AP-1, Stat5, and Creb cooperate in

101 chanism of action involves the activation of transcription factor AP-1 that turns on neuronal growth

102 We focus on the role of the transcription factor AP-1 to both induce the expression

103 Transcription factor AP-1 transduces environmental signa

104 Furthermore, transcription factor AP-1 was a main factor in IL-5-indu

105 The transcription factor AP-1 was involved in the down-regul

106 while antigen receptor-induced activation of transcription factor AP-1 was severely impaired.

107 T cell anergy, in which the activity of the transcription factor AP-1 was substantially diminished.F

108 TNF-induced activation of another nuclear transcription factor, AP-1, was suppressed by IL-13.

109 erentially recruited to binding sites of the transcription factor AP-1, where it represses effector-g

110 nduces cFos phosphorylation, stimulating the transcription factor AP-1, which in turn enhances transc

111 c-Jun is a component of the transcription factor AP-1, which is activated by a wide

112 The transcription factor AP-1, which is composed of Fos and

113 ated ras proteins are potent inducers of the transcription factor AP-1, which is composed of heterodi

114 Jun N-terminal kinase (JNK) regulates the transcription factor AP-1, which is implicated in the co

115 tive in the trnsactivational activity of the transcription factor, AP-1, which is required for optima

116 activity of As3+, we examined its effect on transcription factor AP-1, whose activity is stimulated