ライフサイエンスコーパス: CoCl

1 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(

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

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

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

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

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

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

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

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

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

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

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

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

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

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

16 -1alpha translation was potently elevated by CoCl(2) treatment, as determined by de novo translation

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

58 es shows that the structures containing the [CoCl 4] (2-) anion are contracted along the <101> vector

59 ing the [CoBr 4] (2-) anion for the smaller [CoCl 4] (2-) anion.

60 These include a structure for Tp(t-Bu,Me)CoCl different from that previously reported.

61 tecting group followed by acylation with R(2)COCl introduced the second element of diversity.

62 The ubiquitary Co(I) complex CoCl(PPh3)3 was found to be a convenient catalyst for th

63 Complexes (R,R)-(salcy)CoCl, (R,R)-(salcy)CoBr, (R,R)-(salcy)CoOAc, and (R,R)-(

64 phosphine)iminium) with complex (R,R)-(salcy)CoCl, (R,R)-(salcy)CoBr, or (R,R)-(salcy)CoOBzF(5) resul

65 s then treated with Ac(2)O, BzCl, and PhCH(2)COCl to provide the corresponding meso diesters, 20-22.