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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

26 ensive starting materials (dicyandiamide and CoCl2 ).

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

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

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

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

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

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

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

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

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

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

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

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

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

40 3 or the nonspecific calcium channel blocker CoCl2 partially inhibits the [Ca2+]i increase induced by

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

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

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

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

45 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(

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

47 -1alpha translation was potently elevated by CoCl(2) treatment, as determined by de novo translation

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

65 etabolism were inhibited by cobalt chloride (CoCl2).

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

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

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

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

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

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

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

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

74 1 transcriptional activity induced by either CoCl2 or decreased atmospheric oxygen concentration.

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

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

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

78 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

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

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

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

82 yridyl unit acting as coordinating sites for CoCl2.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

104 0 microM GdCl3, 200 microM NiCl2, 200 microM CoCl2 or 30 microM SKF96365 but was unaffected by additi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

128 Inclusion of CoCl2 during the purification of recombinant UCRP blocks

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

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

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

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

133 were essential for growth in the presence of CoCl2.

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

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

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

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

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

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

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

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

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

143 with a Western diet, lipopolysaccharide, or CoCl2.

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

145 1 activity, and HIF-1alpha overexpression or CoCl2 treatment resulted in elevated IGFBP-1 expression

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

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

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

149 (2% O2), and simulated hypoxia (21% O2 plus CoCl2).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

169 in association with redox responsiveness to CoCl2 treatment.

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

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

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

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

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

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

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

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

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

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

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

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

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

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