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1 ddition to stabilizing the siderophore-bound labile iron pool.
2  was associated with marked reduction of the labile iron pool.
3 f cysteines residues, and an increase in the labile iron pool.
4 1 expression, resulting in a decrease in the labile iron pool.
5 obes for the quantification of intracellular labile iron pools.
6 ione acts as a physiological chelator of the labile iron pool and in which YggX acts upstream of the
7 tation was associated with relatively higher labile iron pool and iron regulatory protein activity th
8                        Both the reduction in labile iron pool and the up-regulation of HIF-1alpha wer
9 e core of this control system, including the labile iron pool as well as proteins that regulate uptak
10 iron supplementation or depletion, including labile iron pools at endogenous, basal levels.
11  TfR expression, and down-regulated cellular labile iron pool by 60%.
12  pool and in which YggX acts upstream of the labile iron pool by preventing superoxide toxicity.
13  be used to identify reversible expansion of labile iron pools by stimulation with vitamin C or the i
14                   Reducing the intracellular labile iron pool decreased parasitism, and antioxidants
15 o a model of ferroptosis reveals a change in labile iron pools during this form of cell death, provid
16  enables ratiometric fluorescence imaging of labile iron pools in living systems.
17  link between the intracellular level of the labile iron pool (LIP) and the susceptibility to UVA-ind
18 ed to be due to subsequent reductions in the labile iron pool (LIP) needed for the synthesis of iron-
19 arametric flow cytometry for quantitation of labile iron pool (LIP) was performed.
20 rotic cell death by moderating the amount of labile iron pool (LIP), but chronic use would cause seve
21 th TNF, this line fails to elevate levels of labile iron pool (LIP), critical for TNF-induced reactiv
22 portion of these species may constitute the "labile iron pool" (LIP) proposed in cellular Fe traffick
23 robe that enables longitudinal monitoring of labile iron pools (LIPs) in living animals.
24 ediated degradation of ferritin, increase in labile iron pool, ROS generation, and/or cell cycle arre
25 tein must scavenge iron from the endogenous, labile iron pool(s).
26 led from iron taken from the BIP-accessible, labile iron pool that is sampled also by ferritin and th
27 n of iron release required an intracellular "labile iron pool" that was rapidly depleted in the prese
28 al iron bound weakly to cellular ligands-the labile iron pool-to generate a response that preserves s
29  ions and is capable of detecting changes in labile iron pools within living cells with iron suppleme

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