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1 ponsive to intracellular iron chelation with desferrioxamine.
2 ontrols who were on long-term treatment with desferrioxamine.
3 by hypoxia and the hypoxia mimics cobalt and desferrioxamine.
4 either cobalt chloride or the iron chelator desferrioxamine.
5 d are either hypoxic or have been exposed to desferrioxamine.
6 henylphenylenediamine, and the iron chelator desferrioxamine.
7 hich is also inducible by the iron chelator, desferrioxamine.
8 ere also induced by exposure of the cells to desferrioxamine.
9 f the inducible response to both hypoxia and desferrioxamine.
10 factor beta (TGF-beta) and the hypoxia mimic desferrioxamine.
11 Lysosomal iron chelation was achieved with desferrioxamine.
12 cally decreased RAGE induction by hypoxia or desferrioxamine.
13 tection was not observed with iron-saturated desferrioxamine.
14 ructurally unrelated chelators dipyridyl and desferrioxamine.
18 rotocol involved treatment of the cells with desferrioxamine, a cell-permeant, Fe(III)-specific chela
19 f intracellular iron-dependent peroxidation, desferrioxamine, abolished the elevation in cellular ROS
21 rioxamine: like hypoxia, cobalt chloride and desferrioxamine activate hypoxia-inducible factor 1alpha
25 n, treatment of cells with the iron chelator desferrioxamine also reduced MLH1 and PMS2 levels, in ke
27 plates that are homogenized and treated with desferrioxamine, an Fe(III) chelator, prior to packing t
28 a-3 PUFA, cotreatment with the iron chelator desferrioxamine, an inhibitor of iron-dependent lipid pe
29 MEL cells, expression of TfR1 was induced by desferrioxamine, an iron chelator, and it was reduced by
30 o inhibited significantly in the presence of desferrioxamine, an iron chelator, but this protection w
33 generation correlated positively with use of desferrioxamine and deferriprone respectively (two studi
35 m/z signals for Th-hydroxamate siderophore (desferrioxamine and ferrichrome) complexes, with Th comp
37 UTR is reduced after treatment of cells with desferrioxamine and increased after interleukin-1 stimul
38 alternatively labeled with (124)I- or (89)Zr-desferrioxamine and injected into mice bearing either ma
39 igands binding to the oxygen sensor, whereas desferrioxamine and perhaps cobalt appear to act at a si
40 ence of transition metal chelators (DTPA +/- desferrioxamine), and was inhibited by catalase, superox
42 2C12 cells to dimethyl oxalylglycine (DMOG), desferrioxamine, and hypoxia, all inhibitors of prolyl h
44 r doses, in combination with the older agent desferrioxamine, and recent trials' data have shown effi
46 ises an iron-specific chelating biomolecule, desferrioxamine B (DFB), covalently immobilized on a mes
47 xperiments with the strong Mn(III) chelator, desferrioxamine B (DFB), in seawater indicated that the
48 preparation and in vivo evaluation of (89)Zr-desferrioxamine B (DFO)-7E11, a novel (89)Zr-labeled mon
49 t study, we report the preparation of (89)Zr-desferrioxamine B (DFO)-J591, a novel (89)Zr-labeled mon
51 by examining the effects of the siderophore desferrioxamine B (DFOB) on Fe removal from aquatic humi
52 ted the potential synergism between ligands (desferrioxamine B (DFOB) or N,N'-Di(2-hydroxybenzyl)ethy
53 lization was found for all ligands examined (desferrioxamine B (DFOB), 2'-deoxymugineic acid (DMA), e
54 tic acid (NTA), iminodiacetic acid (IDA) and desferrioxamine B (DFOB), as well as with Suwannee River
56 he presence of a representative siderophore, desferrioxamine B (DFOB), iron (Fe) was released at high
58 ovel radiolabeled monoclonal antibody (89)Zr-desferrioxamine B [DFO]-J591 for immuno-PET of prostate-
61 hich redox active iron had been removed with desferrioxamine B prevented all of the gpt- mutations ab
62 s complexed with deferoxamine (also known as desferrioxamine B, desferoxamine B), conjugated either t
63 three siderophores of the hydroxamate type: desferrioxamine B, desferrioxamine E, and coelichelin.
67 assays was stimulated by Ni2+, hypoxia, and desferrioxamine, but this activation was not diminished
70 imaging using (89)Zr-DFO-mAb-B43.13 (DFO is desferrioxamine) clearly delineated CA125-positive OVCAR
71 common in the deferiprone group than in the desferrioxamine controls (four [27%] vs 20 [67%], p=0.02
72 odds ratio for excess myocardial iron in the desferrioxamine controls versus the deferiprone group wa
74 n chelating resin, or the chelators EDTA and desferrioxamine decreased monatin and indole loss for so
77 dies indicated that some of the genes in the desferrioxamine (des) and coelichelin (cch) biosynthetic
84 2 mRNA in K562 cells was not up-regulated by desferrioxamine (DFO), a cell membrane-permeable iron ch
85 monstrated with the classical iron chelator, desferrioxamine (DFO), and was not observed for the DFO-
86 Here, we reveal how the iron-binding ligands desferrioxamine (DFO), di-2-pyridylketone-4,4-dimethyl-3
92 laminochroman (2-MAC; 0.3 to 2.5 microM) and desferrioxamine (DFO; 0.25 to 2 mM) reduced cell damage
93 the IEF extract and a siderophore standard (desferrioxamine; DFO) suggested the presence of HS funct
94 amine (SNAP), a nitric oxide (NO) donor, and desferrioxamine (DFx) and cobalt chloride, mimics of cel
96 HIF-1 inducers, cobalt chloride (CoCl2) and desferrioxamine (DFX), on HIF-1 expression and neuroprot
97 tional chelation treatment with subcutaneous desferrioxamine does not prevent excess cardiac iron dep
98 etase superfamily, catalyzes the key step in desferrioxamine E biosynthesis: ATP-dependent trimerisat
100 rescine (HSP) and is structurally related to desferrioxamine E, which is a macrocyclic trimer of N-hy
101 cells exposed to 1% O2, cobalt chloride, or desferrioxamine, each of which also increased levels of
102 e activity and doubling time, whereas Zn and desferrioxamine extended these recoveries and rescued Co
103 e selection of small molecule drugs, such as desferrioxamine (Fe chelator) and clioquinol (Fe, Cu, an
104 re site-specifically conjugated to maleimide-desferrioxamine for (89)Zr radiolabeling and subsequent
107 errichrome has a 5-fold higher affinity than desferrioxamine for Th and a 5-fold lower affinity than
108 e report the novel use of a metallo-complex, desferrioxamine-gallium (DFO-Ga) that targets P. aerugin
113 a phase I dose-escalation study with (89)Zr-desferrioxamine-IAB2M ((89)Zr-IAB2M), an anti-prostate-s
114 find that depletion of intracellular iron by desferrioxamine impairs SFT transport and iron-binding f
119 cells were pretreated with the iron chelator desferrioxamine, indicating a role for iron in inactivat
120 synthesis was inhibited by the iron chelator desferrioxamine, indicating that cytosolic DA and dihydr
122 inepentaacetic acid and, to a lesser extent, desferrioxamine inhibited LDL oxidation when added durin
123 ee alpha-biliverdin yield in the presence of desferrioxamine is significantly increased in the "aged"
124 study, we describe the generation of (89)Zr-desferrioxamine-labeled anti-CD8 cys-diabody ((89)Zr-mal
125 Here we describe the development of (89)Zr-desferrioxamine-labeled transferrin ((89)Zr-transferrin)
126 fective mammalian cells to the iron chelator desferrioxamine leads to degradation of ferritin in the
127 HeLa cells are exposed to the iron chelator desferrioxamine, levels of SFT mRNA increase in an actin
128 using cobalt chloride and the iron chelator desferrioxamine: like hypoxia, cobalt chloride and desfe
129 e (89)Zr-labeled mouse serum albumin ((89)Zr-desferrioxamine-mAlb) as a model radiotracer to assess u
131 s induced by iron can be inhibited by either desferrioxamine mesylate (an iron chelator) or succinyl
132 s shown to be independent of HIF-1alpha, and desferrioxamine mesylate (DFO) and cobalt chloride induc
133 Treatment of PC12 with the iron chelator, desferrioxamine mesylate (DFO, 50 microM for 24 h), sign
134 However, as shown earlier with IRP1, both desferrioxamine mesylate and succinyl acetone will inhib
135 uli: hypoxia (strong) > iron chelation, e.g. desferrioxamine (moderate) >> transition metals, e.g. co
136 introduction of the parenteral iron chelator desferrioxamine more than 30 years ago, 50% of patients
137 methyl-1-pyrroline-1-oxide, the antioxidants desferrioxamine, nordihydroguaiaretic acid, and Amytal,
140 mbient or chemical hypoxia (upon exposure to desferrioxamine or cobalt chloride), an effect that requ
141 tes exceeded that obtained with deferiprone, desferrioxamine, or deferasirox at similar iron-binding
142 h the treatment of hypoxia, cobalt chloride, desferrioxamine, or dimethyloxalyglycine, regardless of
143 In primary human endothelial cells, hypoxia, desferrioxamine, or infection with Ad2/HIF-1alpha/VP16,
146 e that a hydroxylase inhibitor, hypoxia, and desferrioxamine promote the functional and physical inte
152 ligate iron and also by using the chelator, desferrioxamine, that forms a redox-inactive iron comple
153 -fold increase in the level of PfIRPa in the desferrioxamine-treated cultures versus control or iron-
154 und not to alter "free" iron levels, whereas desferrioxamine treatment significantly raised these lev
156 ity by a hydroxylase inhibitor, hypoxia, and desferrioxamine was severely blocked by the adenoviral o
157 so demonstrate responses to both hypoxia and desferrioxamine which are independent of HIF-1 beta and
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