ライフサイエンスコーパス: CoCl(2)

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

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

3 CoCl2 and sirtinol treatment increased Caspase 3 activit

4 CoCl2 concentrations greater than 100 muM resulted in si

5 CoCl2 treatment alone did not significantly affect the r

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

7 CoCl2 treatment increased SIRT1 levels significantly (P<

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

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

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

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

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

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

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

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

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

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

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

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

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

21 ensive starting materials (dicyandiamide and CoCl2 ).

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

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

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

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

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

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

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

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

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

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

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

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

34 3 or the nonspecific calcium channel blocker CoCl2 partially inhibits the [Ca2+]i increase induced by

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

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

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

38 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(

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

40 -1alpha translation was potently elevated by CoCl(2) treatment, as determined by de novo translation

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

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

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

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

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

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

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

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

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

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

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

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

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

54 etabolism were inhibited by cobalt chloride (CoCl2).

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

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

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

58 1 transcriptional activity induced by either CoCl2 or decreased atmospheric oxygen concentration.

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

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

61 yridyl unit acting as coordinating sites for CoCl2.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

78 0 microM GdCl3, 200 microM NiCl2, 200 microM CoCl2 or 30 microM SKF96365 but was unaffected by additi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

97 Inclusion of CoCl2 during the purification of recombinant UCRP blocks

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

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

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

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

102 were essential for growth in the presence of CoCl2.

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

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

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

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

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

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

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

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

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

112 1 activity, and HIF-1alpha overexpression or CoCl2 treatment resulted in elevated IGFBP-1 expression

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

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

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

116 (2% O2), and simulated hypoxia (21% O2 plus CoCl2).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

131 in association with redox responsiveness to CoCl2 treatment.

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

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

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

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

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

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

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

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

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

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

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