ライフサイエンスコーパス: cobalt chloride

1 on and neither does HIF-1alpha activation by cobalt chloride.

2 of DNA condensation reactions with hexammine cobalt chloride.

3 umented in cultured cells in the presence of cobalt chloride.

4 roximately -3.5 kbp mediated the response to cobalt chloride.

5 during the initial 1-h period of exposure to cobalt chloride.

6 In other experiments, cobalt chloride (100 mM) was microinjected near the A7 c

7 Cobalt chloride (100 nM) was then microinjected in the R

8 Desferoxamine and cobalt chloride, 2 compounds that increase the intracell

9 Cobalt chloride (3 mM) prevented, diminished or reversed

10 Cobalt chloride (5 mM; 0.2 or 0.5 microl) injection into

11 Similarly, microinjections of cobalt chloride (a neurotransmission blocker) into the a

12 e deletions sensitive to both low oxygen and cobalt chloride, a hypoxia mimetic.

13 We examined the effect of cobalt chloride, a known stimulator of genes responsive

14 hypoxia (upon exposure to desferrioxamine or cobalt chloride), an effect that requires intact RNA syn

15 nt results in a reduction of the response to cobalt chloride and a complete loss of the response to a

16 iron chelator desferrioxamine: like hypoxia, cobalt chloride and desferrioxamine activate hypoxia-ind

17 Moreover, cobalt chloride and desferrioxamine activated HIF-1 but

18 The hypoxic state can be mimicked by using cobalt chloride and the iron chelator desferrioxamine: l

19 by the nonselective calcium channel blockers cobalt chloride and verapamil, but not by specific organ

20 ble factor (HIF), including desferrioxamine, cobalt chloride, and dimethyloxalylglycine, raised NCOA4

21 egion of the rat glut1 promoter confers both cobalt chloride- and azide-inducibility to a reporter ge

22 s were observed for embryos exposed to 10 mM cobalt chloride (CoCl(2), a chemical inducer of hypoxia-

23 he effect of two other known HIF-1 inducers, cobalt chloride (CoCl2) and desferrioxamine (DFX), on HI

24 ying hypoxic concentrations (100-500 muM) of cobalt chloride (CoCl2) for 24 hours.

25 ctor occurs during hypoxia or in response to cobalt chloride (CoCl2) in Hep3B cells.

26 of HIF-1alpha in MeHg-induced neurotoxicity, cobalt chloride (CoCl2), 2-methoxyestradiol (2-MeOE2), s

27 During chemical hypoxia induced by cobalt chloride (CoCl2), hypoxia-inducible factor 1alpha

28 ytochrome P-450 metabolism were inhibited by cobalt chloride (CoCl2).

29 on control via distinct formation of anionic cobalt chloride complex (CoCl(4)(2-)), while maintaining

30 ffect of HO-1 induction by protoporphyrin IX cobalt chloride (CoPP; a classical inducer of HO-1 expre

31 ical activators of HIF-1 (e.g. deferoxamine, cobalt chloride) could also protect cultured primary neu

32 is diminished with the treatment of hypoxia, cobalt chloride, desferrioxamine, or dimethyloxalyglycin

33 ng mice and exposed to hypoxia-mimetic agent cobalt chloride exhibited less apoptosis and expressed l

34 extract, which was subsequently reacted with cobalt chloride hexahydrate stock solution, leading to t

35 e, nickel sulfate, potassium dichromate, and cobalt chloride identified as the most common allergens.

36 rat liver cell line (Clone 9) to 250 microM cobalt chloride increases GLUT1 mRNA content, which beco

37 lpha, and desferrioxamine mesylate (DFO) and cobalt chloride induced HIF-1alpha but not ATF-4 or GADD

38 hermore, TREX1 expression was enhanced under cobalt chloride-induced hypoxia, leading to a 2-fold red

39 We observed that RACK1 suppressed the cobalt chloride-induced, hypoxia response element-depend

40 isoforms, CGS21680 but not PMA inhibited the cobalt chloride induction of VEGF mRNA.

41 Within 5 min of the cobalt chloride injection, the antinociceptive effect of

42 The induction of GLUT1 mRNA by cobalt chloride is associated with a approximately 10-fo

43 demonstrating that nickel chloride, but not cobalt chloride, is able to stimulate L1 retrotransposit

44 A family of cobalt chloride, methyl, acetylide and hydride complexes

45 nantiopure C(1)-symmetric bis(imino)pyridine cobalt chloride, methyl, hydride, and cyclometalated com

46 sduced with TREX1 constructs with or without cobalt chloride-mimicked hypoxia and HBV replication was

47 de (NO) donor, and desferrioxamine (DFx) and cobalt chloride, mimics of cellular hypoxia, similarly s

48 treated cells, suggesting that the effect of cobalt chloride on GLUT1 mRNA content is largely mediate

49 The effect of cobalt chloride on GLUT1 mRNA content is mimicked by Ni(

50 sed in control cells and in cells exposed to cobalt chloride or azide.

51 Microinjection of cobalt chloride or L-703,606 in the absence of LH stimul

52 HIF-1 activity and Epo expression by either cobalt chloride or the iron chelator desferrioxamine.

53 ishes or Transwell inserts were treated with cobalt chloride or varying doses of IGF-1.

54 ctivation of HIF-1alpha by the hypoxia mimic cobalt chloride, or cell transfection with a degradation

55 ins was increased in cells exposed to 1% O2, cobalt chloride, or desferrioxamine, each of which also

56 proximately 1.5-h half-life of GLUT1 mRNA in cobalt chloride-treated cells, suggesting that the effec

57 ed the HIF-1alpha protein accumulation after cobalt chloride treatment, which was not observed when t

58 pancreatic and prostate carcinoma cell lines cobalt chloride (used to mimic hypoxia) -induced VEGF ex

59 Finally, we demonstrate that cobalt chloride, which also activates HIF-1 and ATF-1/CR

60 The iron chelators desferrioxamine and cobalt chloride, which induce hypoxia-inducible factor (