ライフサイエンスコーパス: CoCl(2)

1 ensive starting materials (dicyandiamide and CoCl2 ).

2 with ZnCl(2) (and to 74% by the addition of CoCl(2)).

3 ed by EDTA and stimulated by the addition of CoCl2.

4 p) were exposed to varying concentrations of COCl2.

5 cidic buffer or the hypoxia-mimicking agent, CoCl2.

6 yridyl unit acting as coordinating sites for CoCl2.

7 were essential for growth in the presence of CoCl2.

8 effect was not mimicked by CaCl2, CdCl2, or CoCl2.

9 or 12 h with 0% or 5% O2 or 300 mum cobalt (CoCl2).

10 etabolism were inhibited by cobalt chloride (CoCl2).

11 (2% O2), and simulated hypoxia (21% O2 plus CoCl2).

12 ependent transcription induced by hypoxia or CoCl(2).

13 thway leading to HIF-1alpha stabilization by CoCl(2).

14 isms for ho-1 gene activation by hypoxia and CoCl(2).

15 etected with exposure of cells to 100 microM CoCl(2).

16 is was also mimicked by exposure of cells to CoCl(2).

17 HeLa cells responding to the hypoxia mimetic CoCl(2).

18 gulate HIF-1alpha translation in response to CoCl(2).

19 d with hypoxia or the hypoxia mimetic agent, CoCl(2).

20 that was activated by addition of ZnCl(2) or CoCl(2).

21 S,S)-2,4-bis-diphenylphosphinopentane (BDPP)]CoCl(2) (0.05 equiv) and methylaluminoxane.

22 cells (MIO-M1) were treated with 100 microM CoCl(2), 1 microg/mL triamcinolone acetonide (TA), or bo

23 aining animals (n = 6/group) were exposed to COCl2 2 ppm x 60 min 1 wk later.

24 lutarate, and ascorbate and was inhibited by CoCl(2), 3,4-dihydroxybenzoate, and 3,4-dihydroxyphenyl

25 increased after intraperitoneal injection of CoCl2 (60 mg/kg) and moderately increased after intraper

26 induced by cobalt(II) chloride hexahydrate (CoCl2.6H2O) and the antineoplastic drug doxorubicin.

27 cellular signaling mechanism of hypoxia- and CoCl2 (a mimetic of hypoxia)-induced IL-8 expression, an

28 or embryos exposed to 10 mM cobalt chloride (CoCl(2), a chemical inducer of hypoxia-inducible factor

29 exposed to 1 mM glutamate in the presence of CoCl(2), a subset of spindle-shaped taste cells accumula

30 tb, and Fpn1) and blocked their induction by CoCl2, a hypoxia mimetic.

31 The importance of HIF-1alpha in insulin- and CoCl2-activated leptin mRNA and protein expression was c

32 ing process involving increased ROS, whereas CoCl2 activates transcription by stimulating ROS generat

33 ut not in control slices that were bathed in CoCl(2) alone, nor in slices that were bathed with the n

34 )pyridine cobalt dihalide complexes ((Ar)PDI)CoCl(2) and ((iPr)BPDI)CoCl(2) ((Ar)PDI = 2,6-(2,6-R(2)-

35 ta showed that pharmacological HIF inducers, CoCl(2) and DFO, did not affect Ang2 expression.

36 Both CoCl(2) and X/XO induced neurite outgrowth in PC12 cells

37 other known HIF-1 inducers, cobalt chloride (CoCl2) and desferrioxamine (DFX), on HIF-1 expression an

38 tion, where hypoxia and the hypoxia mimetics CoCl2 and desferrioxamine (DFO) stabilize it.

39 majority of genes similarly affected by both CoCl2 and low oxygen were involved in ergosterol synthes

40 dependant gene activation in the presence of CoCl2 and low oxygen.

41 anol completely suppressed ROS generation by CoCl2 and NiCl2 but did not diminish the induced Cap43 g

42 cells increase ROS generation in response to CoCl2 and retain the ability to induce expression of the

43 CoCl2 and sirtinol treatment increased Caspase 3 activit

44 ipitation experiments revealed that insulin, CoCl2 and/or hypoxia treatments augmented nuclear accumu

45 bidentate phosphine-CoCl(2) complexes {[P~P](CoCl(2))} and Me(3)Al in an atmosphere of ethylene.

46 with other oxidative stresses, including UV, CoCl(2), and H(2)O(2) treatments.

47 de complexes ((Ar)PDI)CoCl(2) and ((iPr)BPDI)CoCl(2) ((Ar)PDI = 2,6-(2,6-R(2)-C(6)H(3)N=CMe)(2)C(5)H(

48 mM HEPES buffer with 100 mM NaCl and 0.05 mM CoCl2 at 30 degrees C.

49 indeed generated in D54-MG cells exposed to CoCl2 but it was unlikely that ROS participated in the h

50 -diene with (S,S)-(DIOP)CoCl2 or (S,S)-(BDPP)CoCl2 catalyst in the presence of Me3Al, the (E)-isomer

51 howed higher XO activity in cells exposed to CoCl2 compared with cells grown in normoxia.

52 nd concomitant treatment with both GdCl3 and CoCl2 completely inhibits the field-induced [Ca2+]i incr

53 ith catalytic amounts of bidentate phosphine-CoCl(2) complexes {[P~P](CoCl(2))} and Me(3)Al in an atm

54 orylated SAPK/JNK increased 36-fold (200 muM CoCl2 concentration), then plateaued at the 300- (25-fol

55 t the 300- (25-fold) and 400-muM (27.8-fold) CoCl2 concentrations (P<0.01).

56 ificantly higher than control at the 100-muM CoCl2 concentrations (P<0.01).

57 ast cells sense and adapt to changes in both CoCl2 concentrations and oxygen levels.

58 CoCl2 concentrations greater than 100 muM resulted in si

59 n when exposed to CdCl(2), ZnSO(4), NiCl(2), CoCl(2), CuCl(2), heat, UV-B and carbofuron showed incre

60 gy and cytoskeleton arrangement triggered by CoCl2; decreased the expression of vimentin and fibronec

61 One millimolar of CoCl2 depressed, or blocked, the effects of Na2S2O4 on [

62 Normoxic inducers of HIF (CoCl(2), desferrioxamine, and l-mimosine) and 100 ng/ml

63 those rats that had inhaled higher doses of COCl2 during the first exposure.

64 Inclusion of CoCl2 during the purification of recombinant UCRP blocks

65 The metalation of Zr12-TPDC SBUs with CoCl2 followed by treatment with NaBEt3H afforded a high

66 Reduction with SmI2, treatment with COCl2, followed by OMB deprotection gave diastereomerica

67 The metalation of Zr-MTBC SBUs with CoCl2, followed by treatment with NaBEt3H, afforded high

68 entrations (100-500 muM) of cobalt chloride (CoCl2) for 24 hours.

69 duced by hypoxia ( approximately 1% O(2)) or CoCl(2) (hypoxia mimic), similarly to that for TGF-beta-

70 chemical hypoxia induced by cobalt chloride (CoCl2), hypoxia-inducible factor 1alpha (HIF1-alpha) med

71 parameter changes due to the hypoxia mimetic CoCl(2) in the p53 mutated SKNBE2(c) human neuroblastoma

72 Sodium amalgam reduction of CoCl(2) in the presence of CNAr(Mes2) provides the salt

73 g hypoxia or in response to cobalt chloride (CoCl2) in Hep3B cells.

74 wild-type cells, and abolish the response to CoCl2 in rho degrees cells.

75 estigated the effects of the hypoxia-mimetic CoCl2 in the pathogenic fungus Cryptococcus neoformans a

76 activation of these genes during hypoxia or CoCl2 in wild-type cells, and abolish the response to Co

77 with IL-8 promoter revealed that hypoxia and CoCl2 increased DNA-binding activity of hypoxia-inducibl

78 Although treatment with NiCl2 and CoCl2 increased the activity of H265V CODH by severalfol

79 We showed that CoCl2 increased xanthine oxidase (XO)-derived reactive o

80 e ROS generation during hypoxia (1.5% O2) or CoCl2 incubation, (ii) Hep3B cells depleted of mitochond

81 veral HIF-1 binding sites were necessary for CoCl(2)-induced expression of the Hsp27 gene.

82 Here, we report that during CoCl(2)-induced hypoxic stress, HuR is significantly ove

83 pper transport protein, Ctr1, also inhibited CoCl2-induced EMT and reversed the mesenchymal phenotype

84 These results indicate that TEPA inhibits CoCl2-induced EMT most likely via HIF1-alpha-Snail/Twist

85 Using CoCl2-induced EMT of human breast carcinoma MCF-7 cells,

86 In addition, we show that hypoxia- and CoCl2-induced IL-8 expression requires activation of HIF

87 We show that hypoxia- and CoCl2-induced IL-8 mRNA and protein expression involved

88 eins were found to bind HIF-1alpha mRNA in a CoCl(2)-inducible manner as assessed by immunoprecipitat

89 er the development of tolerance of phosgene (COCl2) is associated with a decreased incursion of neutr

90 ere studied: (1) sham-operated; (2) 50 mg of CoCl2/kg subcutaneously for 2 d; (3) acute hypertension

91 ryptococcus neoformans and demonstrated that CoCl2 leads to defects in several enzymatic steps in erg

92 sence of hypoxia-mimicking concentrations of CoCl(2), mitochondrial but not nuclear DNA damage is ind

93 of flowering, and have enhanced tolerance to CoCl(2), molybdic acid, ZnSO(4), and MgCl(2).

94 We show that the inhibitory effect of CoCl2 on scp1Delta and sre1Delta cells likely resulted f

95 biosynthesis inhibitors, succinylacetone and CoCl2 on the cytochrome c oxidase (COX) gene expression

96 omyces pombe, suggesting that the effects of CoCl2 on the Sre1p-mediated response are conserved in fu

97 Cultured retinal cells were treated with CoCl(2) or 2% O(2) to induce hypoxia.

98 In normal PASMCs, HIF-1alpha activation by CoCl(2) or desferrioxamine causes DRP1-mediated fission.

99 DIT4 in response to metformin, hypoxia-like (CoCl2) or genotoxic stress.

100 xposure of cells to divalent metals (such as CoCl2) or iron chelators [such as desferrioxamine (DFO)]

101 of a prototypical 1,3-diene with (S,S)-(DIOP)CoCl2 or (S,S)-(BDPP)CoCl2 catalyst in the presence of M

102 0 microM GdCl3, 200 microM NiCl2, 200 microM CoCl2 or 30 microM SKF96365 but was unaffected by additi

103 1 transcriptional activity induced by either CoCl2 or decreased atmospheric oxygen concentration.

104 Preconditioning with CoCl2 or DFX 24 hours before hypoxia-ischemia afforded 7

105 Rat CSM cells in vitro were treated with CoCl2 or low oxygen tension to mimic hypoxia.

106 oses of insulin or the hypoxia-mimetic agent CoCl2, or culturing the cells under hypoxic conditions s

107 NA expression, whereas induction by hypoxia, CoCl2, or DFO was unaffected.

108 nct from mechanisms of induction by hypoxia, CoCl2, or DFO.

109 nous EPO mRNA expression induced by hypoxia, CoCl2, or DFO.

110 3 or the nonspecific calcium channel blocker CoCl2 partially inhibits the [Ca2+]i increase induced by

111 The system CoCl(2)/Pr(i)(3)P/(Me(3)Si)(2)S/THF assembles [Co(4)S(4)

112 a mimetics such as deferoxamine mesylate and CoCl(2), regardless of their HIF-alpha protein expressio

113 Succinylacetone and CoCl2 showed tissue-specific differences in their abilit

114 In Ka13 cells, CoCl(2) stimulated expression of a luciferase reporter g

115 All currents were blocked by 1 mM CoCl2 suggesting that, at this concentration, cobalt exe

116 k chorioallantoic membranes and treated with CoCl(2), to model hypoxia, demonstrate increased dissemi

117 HIF-1alpha levels increased dramatically in CoCl(2)-treated cells, while HIF-1alpha mRNA levels were

118 In non-CoCl2-treated animals, acute hypertension provoked a thr

119 In CoCl2-treated animals, acute urine output and endogenous

120 an hepatoma cells and repressed threefold by CoCl(2) treatment in rabbit corneal stromal and epitheli

121 in normoxic condition in vitro, hypoxia and CoCl(2) treatment increased Epo secretion.

122 -1alpha translation was potently elevated by CoCl(2) treatment, as determined by de novo translation

123 nd the production of extracellular S1P after CoCl(2) treatment, whereas HIF-1alpha small interfering

124 ated in its translational upregulation after CoCl(2) treatment.

125 ot further induce translation in response to CoCl(2) treatment.

126 CoCl2 treatment alone did not significantly affect the r

127 for 5 min; and (4) acute hypertension after CoCl2 treatment as in group 3.

128 These findings demonstrate that CoCl2 treatment both attenuates the inhibition of proxim

129 CoCl2 treatment for 8 h, however, selectively affected t

130 CoCl2 treatment increased SIRT1 levels significantly (P<

131 1 activity, and HIF-1alpha overexpression or CoCl2 treatment resulted in elevated IGFBP-1 expression

132 in level increased in response to hypoxia or CoCl2 treatment, whereas HIFalpha Ib, Ic, and Id showed

133 in association with redox responsiveness to CoCl2 treatment.

134 ep-a) was up-regulated upon both hypoxia and CoCl(2) treatments.

135 CoCl(2) upregulated Hsp27 in cultured retinal neurons.

136 Furthermore, CoCl(2) upregulated Hsp27 in the rat retina and protecte

137 del of retinal ischemia to determine whether CoCl(2) upregulates rHsp27 and protects the retina from

138 response to hypoxia and the hypoxia-mimetic CoCl(2) was similar to that observed in wild type (K1) c

139 e steady state generation of superoxide, and CoCl(2) was used as a representative transition metal re

140 CoCl(2) was used to test for Hsp27 expression after hypo

141 ha expression and translation in response to CoCl(2) were markedly elevated after HuR overexpression.

142 and 6-fold, respectively, by treatment with CoCl2, whereas low oxygen tension caused increases in ex

143 r glutamate (0.5 or 1 mM) in the presence of CoCl(2), which can pass into cells through the ligand-ga

144 iate stimulation by dioxin and repression by CoCl(2), which simulates hypoxia.

145 en LRP-1-silenced CL16 cells were exposed to CoCl2, which models changes that occur in hypoxia.

146 mTOR enhanced HIF-1 activation by hypoxia or CoCl(2), while expression of a rapamycin-resistant mTOR

147 The air-free reaction of CoCl2 with 1,3,5-tri(1H-1,2,3-triazol-5-yl)benzene (H3BT