ライフサイエンスコーパス: CoCl(2)

1 ensive starting materials (dicyandiamide and CoCl2 ).

2 receptor damage caused by a specific dose of CoCl(2) .

3 th and progenitor proliferation induced with CoCl(2) .

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

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

6 p) were exposed to varying concentrations of COCl2.

7 yridyl unit acting as coordinating sites for CoCl2.

8 with a Western diet, lipopolysaccharide, or CoCl2.

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

10 were essential for growth in the presence of CoCl2.

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

12 etabolism were inhibited by cobalt chloride (CoCl2).

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

14 (2% O2), and simulated hypoxia (21% O2 plus CoCl2).

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

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

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

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

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

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

21 onolayer two-dimensional (2D) semiconductor, CoCl(2).

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

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

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

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

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

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

28 MeHg-induced neurotoxicity, cobalt chloride (CoCl2), 2-methoxyestradiol (2-MeOE2), small interfering

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

30 binding constants of K(LF) = 88.5 M(-1) for CoCl(2), 52.7 M(-1) for MnCl(2), and 49.7 M(-1) for NiCl

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

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

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

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

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

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

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

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

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

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

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

42 and chemicals known to stabilise HIF-1alpha (CoCl(2) and DMOG) on bone formation.

43 Interestingly, both hypoxia mimetics (CoCl(2) and DMOG) partly restored hyperglycaemia inhibit

44 bit sorption capacities, Q = 1.33 mmol/g for CoCl(2) and Q = 0.66 mmol/g for Co(NO(3))(2), as inferre

45 identifies the rich category of polarons in CoCl(2) and their feasibility of precise control unprece

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

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

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

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

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

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

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

53 CoCl2 and sirtinol treatment increased Caspase 3 activit

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

55 mononuclear cells incubation with NiSO(4) , CoCl(2) , and PdCl(2) increased frequencies of CD154 + C

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

57 ol and DeltaS degrees = 56.0 J/K.mol for L + CoCl(2), and DeltaH degrees = 16.5 kJ/mol and DeltaS deg

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

59 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(

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

61 ce of cobalt(II)-salts like Co(ClO(4))(2) or CoCl(2) bind the second Co(II)-ion; further internal ele

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

63 A heat-driven catch-and-release strategy for CoCl(2) capture is described.

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

65 e report an unprecedented microwave-assisted CoCl(2)-catalyzed acceptorless dehydrogenative coupling

66 isotope effect reveal the mechanism of this CoCl(2-)catalyzed reaction to be via ADC.

67 Ion chromatographic analysis of a mixed CoCl(2)/Co(NO(3))(2) solution revealed an increase in ch

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

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

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

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

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

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

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

75 CoCl2 concentrations greater than 100 muM resulted in si

76 II) chloride (FeCl(2)), cobalt(II) chloride (CoCl(2)), copper(I) chloride (CuCl)] are effective catal

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

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

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

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

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

82 Inclusion of CoCl2 during the purification of recombinant UCRP blocks

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

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

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

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

87 The complex, (dppp)CoCl(2), gives the best results (ratio of 1,2- to 1,4-ad

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

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

90 A catalyst system comprising CoCl(2)/IAd.HBF(4) enables the Suzuki-Miyaura cross-coup

91 and DeltaS degrees = 85.0 J/K.mol for PS-L + CoCl(2) in 95% ethanol.

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

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

94 Metalation of ((Tr)L)Li with CoCl(2) in THF afforded a high-spin (S = 3/2) three-coor

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

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

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

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

99 RL/MpJ MDSPCs with dimethyloxalylglycine and CoCl(2) increased the expression of HIF-1alpha and targe

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

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

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

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

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

105 the effects of etoposide-induced DNA damage, CoCl(2)-induced hypoxia, and 5' cap inhibition with 4EGI

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

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

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

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

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

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

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

113 In CoCl(2) -injured retinas, blockade of endogenous extrace

114 was established via applying hypoxia mimetic CoCl(2), iron chelator desferrioxamine, proteasome inhib

115 spin states and metallization in compressed CoCl(2) is investigated by combining diffraction, resist

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

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

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

119 s, that can be simulated with treatment with CoCl(2), leads to an increase in glycolysis, and more da

120 Additionally, both CoCl(2)-mimicked hypoxia and suppression of endogenous S

121 tion of HTR-8 cell migration and invasion by CoCl(2)-mimicked hypoxia was through the SRC-3/AKT/mTOR

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

123 a simulated ion mixture containing equimolar CoCl(2), MnCl(2), and NiCl(2), ICP-MS analyses served to

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

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

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

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

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

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

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

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

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

133 0 microM GdCl3, 200 microM NiCl2, 200 microM CoCl2 or 30 microM SKF96365 but was unaffected by additi

134 1 transcriptional activity induced by either CoCl2 or decreased atmospheric oxygen concentration.

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

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

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

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

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

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

141 n EC exposed to CoCl(2) , P. gingivalis, and CoCl(2) + P. gingivalis (p < 0.05).

142 sed to CoCl(2), P. gingivalis (MOI 100), and CoCl(2) + P. gingivalis was evaluated through hypoxia de

143 IF-1alpha, and MMP-9 levels in EC exposed to CoCl(2) , P. gingivalis, and CoCl(2) + P. gingivalis (p

144 tus in oral epithelial cells (EC) exposed to CoCl(2), P. gingivalis (MOI 100), and CoCl(2) + P. gingi

145 3 or the nonspecific calcium channel blocker CoCl2 partially inhibits the [Ca2+]i increase induced by

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

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

148 iffraction analysis of a single crystal of L.CoCl(2) revealed an ion-pair complex comprising a hexaco

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

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

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

152 manipulation of single polarons in monolayer CoCl(2), that are grown on HOPG substrate via molecular

153 In supplemented minimal media containing CoCl(2), the metabolically produced CoPPIX is directly i

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

155 The device was used to enrich CoCl(2) treated MDA-MB 231 breast cancer cells from an u

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

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

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

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

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

161 -1alpha translation was potently elevated by CoCl(2) treatment, as determined by de novo translation

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

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

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

165 CoCl2 treatment alone did not significantly affect the r

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

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

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

169 CoCl2 treatment increased SIRT1 levels significantly (P<

170 1 activity, and HIF-1alpha overexpression or CoCl2 treatment resulted in elevated IGFBP-1 expression

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

172 in association with redox responsiveness to CoCl2 treatment.

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

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

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

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

177 binding and release of cobalt(II) chloride (CoCl(2)) via a solvent polarity switch mechanism involvi

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

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

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

181 By subjecting TE-tagged cells to CoCl(2), we found the TE integration provided the major

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

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

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

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

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

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

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