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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.
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
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 egion of the rat glut1 promoter confers both cobalt chloride- and azide-inducibility to a reporter ge
21 s were observed for embryos exposed to 10 mM cobalt chloride (CoCl(2), a chemical inducer of hypoxia-
22 he effect of two other known HIF-1 inducers, cobalt chloride (CoCl2) and desferrioxamine (DFX), on HI
27 ffect of HO-1 induction by protoporphyrin IX cobalt chloride (CoPP; a classical inducer of HO-1 expre
28 ical activators of HIF-1 (e.g. deferoxamine, cobalt chloride) could also protect cultured primary neu
29 is diminished with the treatment of hypoxia, cobalt chloride, desferrioxamine, or dimethyloxalyglycin
30 ng mice and exposed to hypoxia-mimetic agent cobalt chloride exhibited less apoptosis and expressed l
31 rat liver cell line (Clone 9) to 250 microM cobalt chloride increases GLUT1 mRNA content, which beco
32 lpha, and desferrioxamine mesylate (DFO) and cobalt chloride induced HIF-1alpha but not ATF-4 or GADD
37 demonstrating that nickel chloride, but not cobalt chloride, is able to stimulate L1 retrotransposit
39 nantiopure C(1)-symmetric bis(imino)pyridine cobalt chloride, methyl, hydride, and cyclometalated com
40 de (NO) donor, and desferrioxamine (DFx) and cobalt chloride, mimics of cellular hypoxia, similarly s
41 treated cells, suggesting that the effect of cobalt chloride on GLUT1 mRNA content is largely mediate
45 HIF-1 activity and Epo expression by either cobalt chloride or the iron chelator desferrioxamine.
47 ctivation of HIF-1alpha by the hypoxia mimic cobalt chloride, or cell transfection with a degradation
48 ins was increased in cells exposed to 1% O2, cobalt chloride, or desferrioxamine, each of which also
49 proximately 1.5-h half-life of GLUT1 mRNA in cobalt chloride-treated cells, suggesting that the effec
50 ed the HIF-1alpha protein accumulation after cobalt chloride treatment, which was not observed when t
51 pancreatic and prostate carcinoma cell lines cobalt chloride (used to mimic hypoxia) -induced VEGF ex
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