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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
9 e core of this control system, including the labile iron pool as well as proteins that regulate uptak
13 be used to identify reversible expansion of labile iron pools by stimulation with vitamin C or the i
15 o a model of ferroptosis reveals a change in labile iron pools during this form of cell death, provid
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-
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
24 ediated degradation of ferritin, increase in labile iron pool, ROS generation, and/or cell cycle arre
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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