ライフサイエンスコーパス: CT-1

1 CT-1 action on motoneurons was inhibited by phosphatidyl

2 CT-1 also induced the degradation of the NF-kappa B cyto

3 CT-1 and gp130/LIF receptor were widely present in the c

4 CT-1 and IGF-I may be considered promising candidate tro

5 CT-1 induces a distinct pattern of immediate early genes

6 CT-1 induces a hypertrophic response in cardiomyocytes t

7 CT-1 is a new member of the interleukin 6 (IL-6)/leukemi

8 CT-1 is highly expressed in embryonic skeletal muscle, s

9 CT-1 is released from the heart in response to hypoxic s

10 CT-1 is the first bona fide muscle-derived neurotrophic

11 CT-1 may be important in normal motoneuron development a

12 CT-1 was injected through the penile vein 30 min before

13 CT-1, however, follows a strict degradation pathway afte

14 Cardiotrophin 1 (CT-1), a potent cardiac survival factor, is capable of i

15 otrophic factor (BDNF), and cardiotrophin-1 (CT-1) are the most potent neurotrophic factors for moton

16 Cardiotrophin-1 (CT-1) is a potent hypertrophic factor discovered by coup

17 systemic administration of cardiotrophin-1 (CT-1) is able to improve renal function and to decrease

18 Cardiotrophin-1 (CT-1) was recently isolated by expression cloning based

19 Cardiotrophin-1 (CT-1), a cytokine related to ciliary neurotrophic factor

20 Cardiotrophin-1 (CT-1), a member of the interleukin-6 superfamily, and en

21 Cardiotrophin-1 (CT-1), a stress-induced cytokine, belongs to the interle

22 isolated a novel cytokine, cardiotrophin-1 (CT-1), from an in vitro embryonic stem cell system of ca

23 rotrophic factor (CNTF), or cardiotrophin-1 (CT-1).

24 otrophic factor (CNTF), and cardiotrophin-1 (CT-1).

25 the CNTF-LIF family member cardiotrophin-1 (CT-1).

26 After E12.5, CT-1 expression is found in other tissues, including ske

27 have developed antibodies directed against a CT-1 fusion protein.

28 At PD20, a CT-1-treated eye (2 micro g/2 micro L every 3 days, star

29 However, acute CT-1 treatment caused an increase in SOCS-3 mRNA in adip

30 un to the SPRR1A promoter was observed after CT-1 stimulation.

31 sphorylated STAT1 and -3 in the retina after CT-1 injection.

32 Although CT-1 and ET-1 gene expression in the heart is upregulate

33 RAP-alpha1 variant, which contains NT-1 and CT-1 domains, and T-cell responses were characterized.

34 mice demonstrated increased alpha-actin and CT-1 mRNA expression, and airway myocytes isolated from

35 from the tongue radiolabeled GDNF, BDNF, and CT-1 as well as tetanus toxin.

36 LIF, CNTF, and CT-1 act through the known receptors LIF receptor beta (

37 eral of these cytokines (LIF, OSM, CNTF, and CT-1) also utilize the LIF receptor (LIFR) as a componen

38 directed against endogenous IGF-I, GDNF, and CT-1, significantly decreased mean single-twitch force.

39 d at synapses more slowly (within 15 h), and CT-1 never associated with synapses.

40 in expression induced by LiCl, SB216763, and CT-1 but not TGF-beta.

41 in adipose tissue of both wild-type (WT) and CT-1(-/-) mice.

42 F receptor inhibited basal growth as well as CT-1- or ET-1-stimulated cardiac fibroblast growth.

43 The median CVS at CT 1 was 5; at CT 2, 4; and at US, 4.

44 derwent all three studies, the median CVS at CT 1 was 5; at CT 2, 4; and at US, 4.

45 Factors related to CVS at CT 1 were homogeneous versus heterogeneous appearance (s

46 ion, we investigated the interaction between CT-1/gp130/LIF receptor and ET-1/endothelin type A (ET(A

47 eIF2Bepsilon siRNA also blocked CT-1- but not TGF-beta-induced protein synthesis.

48 Together, the inhibitors completely blocked CT-1-dependent NF-kappa B activation and cytoprotection.

49 Both CT-1 and LIF, which share the same receptors, dramatical

50 by nuclear run-on transcription assays, both CT-1 and alpha-adrenergic stimulation lead to an increas

51 A partial remission was seen by CT 1 mo after the first radioimmunotherapy, and a furthe

52 e essential for cardiac fibroblast growth by CT-1 and that there is synergism with ET-1/ET(A) recepto

53 kinases, whereas the hypertrophy induced by CT-1 may be mediated by alternative pathways, e.g. Janus

54 ibody completely inhibits c-fos induction by CT-1.

55 Cardiotrophin (CT-1) is a naturally occurring protein member of the int

56 ), Interleukin-11 (IL-11) and Cardiotrophin (CT-1).

57 Moreover, chronic CT-1 treatment resulted in the development of insulin re

58 ice and characterization of 24-h circulating CT-1 profiles in normal-weight and overweight/obese subj

59 therapy, all patients underwent planning CT (CT 1) at 3-mm section intervals.

60 9), followed by DeALPS-CT-2 (588) and DeALPS-CT-1 (330).

61 levels of IgG anti-LPS (DeALPS-CT-2 > DeALPS-CT-1 > cellular vaccine).

62 was disrupted in aged obese CT-1-deficient (CT-1(-/-)) mice (12 mo).

63 binding of CT-1 to CNTFR alpha was detected, CT-1 may use a novel cytokine receptor alpha subunit.

64 ere absorbed (>75%) by LPS but not by either CT-1 or CT-2.

65 d by an Ab directed at a C-terminal epitope (CT-1) but not with an Ab recognizing a protected intralu

66 Exogenous CT-1 markedly stimulated [(3)H]thymidine and [(3)H]proli

67 cells stimulated by endogenous and exogenous CT-1 requires gp130/LIF receptor as well as ET(A) recept

68 but not bovine insulin-primed CTL expressed CT-1, a carbohydrate epitope of CD45, and bovine insulin

69 either to increase levels of trophic factors CT-1, IGF-I, glial cell line-derived neurotrophic factor

70 t study documents that gp130 is required for CT-1 signaling in cardiomyocytes, by demonstrating that

71 -kappa B and that NF-kappa B is required for CT-1 to mediate its full cytoprotective effects in cardi

72 se observations suggest a potential role for CT-1 in the regulation of metabolic circadian rhythms.

73 In the heart, CT-1 is primarily expressed in myocardial cells, and not

74 In humans, CT-1 plasma profile exhibited a 24-h circadian rhythm in

75 As assessed by immunolocalization, CT-1 is predominantly expressed in the early mouse embry

76 However, the pattern was altered in CT-1(-/-) mice toward a lower percentage of the rhythm o

77 r antagonist, BQ123, significantly inhibited CT-1-stimulated DNA synthesis.

78 rhythms of Vo2 were conserved in young lean CT-1(-/-) mice (2 mo), CT-1 deficiency caused a phase sh

79 nserved in young lean CT-1(-/-) mice (2 mo), CT-1 deficiency caused a phase shift of the acrophase.

80 Moreover, CT-1 mRNA levels in adipose tissue showed significant ci

81 Our studies revealed that neither CT-1 nor ciliary neurotrophic factor treatment affected

82 ption rate (Vo2) was disrupted in aged obese CT-1-deficient (CT-1(-/-)) mice (12 mo).

83 We also confirmed the ability of CT-1 to induce signaling in fat cells in vivo.

84 nal cell survival, we studied the ability of CT-1 to promote cardiac myocyte survival and proliferati

85 igned to identify the presence and action of CT-1 and its receptor complex, glycoprotein130 (gp130) a

86 Repeated administration of CT-1 resulted in significant survival of photoreceptors.

87 Chronic administration of CT-1 to 3T3-L1 adipocytes resulted in a decrease of both

88 Since no binding of CT-1 to CNTFR alpha was detected, CT-1 may use a novel c

89 AP kinase pathway for the survival effect of CT-1.

90 AP kinase, as well as the survival effect of CT-1.

91 on, as well as the cytoprotective effects of CT-1 against hypoxic stress.

92 family cytokines, we examined the effects of CT-1 on 3T3-L1 adipocytes.

93 The effects of CT-1 on SOCS-3 and PPARgamma mRNA were independent of MA

94 These effects of CT-1 seem to be mediated by reduction in oxygen-radical

95 l cells blocked the antiapoptotic effects of CT-1, indicating a requirement of the MAP kinase pathway

96 tely inhibited the cytoprotective effects of CT-1.

97 e the developmental pattern of expression of CT-1 during murine embryogenesis, we have developed anti

98 Confocal laser microscopy of CT-1 stimulated cells reveals the assembly of sarcomeric

99 The 24-h pattern of CT-1 was characterized by a pronounced increase during t

100 c response elicited following stimulation of CT-1.

101 ces the B subunit (but not the A subunit) of CT-1.

102 t a subset of gp130 cytokines, in particular CT-1, LIF, and OSM, has the ability to impair subsequent

103 PET/CT-1 was compared with routine staging, and response on

104 PET/CT was performed at baseline (PET/CT-1) and after 3 cycles of neoadjuvant chemotherapy (PE

105 o have uptake in cervical lymph nodes on PET/CT-1, and 2 of 3 IRSS stage IIIB patients with pathologi

106 7 patients without optic nerve uptake on PET/CT-1.

107 All 25 patients underwent PET/CT-1, and 21 of 25 patients underwent PET/CT-2.

108 Moreover, the circadian pattern of plasma CT-1 levels was evaluated in normal-weight and overweigh

109 Recombinant CT-1 was injected intravitreally into eyes of heterozygo

110 ERK, or Akt pathways each partially reduced CT-1-mediated NF-kappa B activation, as well as the cyto

111 PI was followed by SPECT/CT 1-3 h after injection of (99m)Tc-colloid particles.

112 In the present study, CT-1 activated p38 and ERK MAPKs as well as Akt in cultu

113 In summary, CT-1 is a potent regulator of signaling in adipocytes in

114 ell epitopes may vary antigenically and that CT-1 may be differentially expressed with respect to the

115 Northern blot analysis demonstrated that CT-1 gene expression was present in normal atrium and ve

116 This study demonstrates that CT-1 and its receptors are present in cardiac fibroblast

117 ponsible for this effect, we documented that CT-1 activated both signal transducer and activator of t

118 A cell proliferation assay documents that CT-1 provokes an approximate 2-fold increase in embryoni

119 sphorylated, providing further evidence that CT-1 signals through the gp130/LIFRbeta heterodimer in c

120 These studies indicate that CT-1 can activate a distinct form of myocardial cell hyp

121 These results indicate that CT-1 promotes photoreceptor survival and that Muller cel

122 These results indicate that CT-1 signals through p38, ERK, and Akt in a parallel man

123 Our studies have shown that CT-1 administration results in a dose- and time-dependen

124 Therefore, these results suggest that CT-1 administration prevents IRI and it might be used as

125 Sequence similarity data suggested that CT-1 is a novel member of a family of structurally relat

126 fic phospholipase C (PIPLC), suggesting that CT-1 may act through a GPI-linked component.

127 cavity volume decreased somewhat during the CT 1-to-CT 2 interval.

128 (LIFRbeta) antagonist effectively blocks the CT-1 induction of c-fos, indicating a requirement for LI

129 The T-cell epitope in the CT-1 domain was mapped to aa 436 to 465 (VNSEKVDADDAGNAE

130 Survival in the CT-1-treated group was higher than in the untreated grou

131 ontrast to alpha-adrenergic stimulation, the CT-1 responsive cis-regulatory elements are located outs

132 cids [aa] 144 to 187), and one mapped to the CT-1 variable domain (aa 386 to 480).

133 Therefore, CT-1 promotes cardiac myocyte survival via the activatio

134 Thus, CT-1 may play an autocrine role during cardiac chamber g

135 ter; none of these were changed at follow-up CT 1 year later.

136 hymic masses, 25 were evaluated at follow-up CT 1 year later: Five had increased in diameter, two had

137 rotype Inaba, to cholera toxin (CT) variants CT-1 and CT-2.

138 tential activation of atrial and ventricular CT-1 expression in pacing-induced experimental congestiv

139 s a positive correlation between ventricular CT-1 mRNA and left ventricular mass index.

140 In vitro, CT-1 kept 43% of purified E14 rat motoneurons alive for

141 In vivo, CT-1 protected neonatal sciatic motoneurons against the

142 In the present study, we analyzed whether CT-1 also acts to peripherally regulate metabolic rhythm

143 Stimulation with CT-1 results in an increase in cardiac cell size that is

144 Upon stimulation with CT-1, both gpl30 and the LIFRbeta are tyrosine-phosphory

145 Treatment with CT-1 or IGF-I significantly increased the mean single-tw