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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 n, and mitochondrial flux in controlling the labile iron pool.
5 pression by limiting the availability of the labile iron pool.
6 n and a corresponding change in the cellular labile iron pool.
7 insically fluorescent nuclear tracer for the labile iron pool.
8 1 expression, resulting in a decrease in the labile iron pool.
9 obes for the quantification of intracellular labile iron pools.
10 s, resulting in excessive ROS production and labile iron pool accumulation.
11 ione acts as a physiological chelator of the labile iron pool and in which YggX acts upstream of the
12 tation was associated with relatively higher labile iron pool and iron regulatory protein activity th
13                        Both the reduction in labile iron pool and the up-regulation of HIF-1alpha wer
14                                By connecting labile iron pools and NRF2-ARE activity to a druggable m
15 acity to disrupt GPX4 stability, elevate the labile iron pool, and intensify lipid peroxidation, ulti
16  that the added (57)Fe initially entered the labile iron pool, and then distributed to vacuoles and m
17       Finally, cellular iron storage and the labile iron pool are maintained via autophagic degradati
18 onitor loosely bound Fe(II) ions, termed the labile iron pool, are potentially powerful tools for stu
19 e core of this control system, including the labile iron pool as well as proteins that regulate uptak
20 iron supplementation or depletion, including labile iron pools at endogenous, basal levels.
21  TfR expression, and down-regulated cellular labile iron pool by 60%.
22  pool and in which YggX acts upstream of the labile iron pool by preventing superoxide toxicity.
23  be used to identify reversible expansion of labile iron pools by stimulation with vitamin C or the i
24                   Reducing the intracellular labile iron pool decreased parasitism, and antioxidants
25 o a model of ferroptosis reveals a change in labile iron pools during this form of cell death, provid
26  ferritinophagy, rescued cell growth and the labile iron pool in PINK1 KD cells.
27 ron storage protein ferritin and a decreased labile iron pool in the PINK1 KD cells, but total cellul
28          However, measurement of kinetically labile iron pools in enteroids competent or blocked for
29 nd labeling strategy that enables imaging of labile iron pools in live cells through enhancement in c
30  enables ratiometric fluorescence imaging of labile iron pools in living systems.
31                             The existence of labile iron pools (LFePs) in biological systems has been
32  link between the intracellular level of the labile iron pool (LIP) and the susceptibility to UVA-ind
33                     DMT1 silencing increases labile iron pool (LIP) levels and activates PINK1/Parkin
34 ed to be due to subsequent reductions in the labile iron pool (LIP) needed for the synthesis of iron-
35 tically, by targeting the expanded cytosolic labile iron pool (LIP) of the cancer cell.
36                  Enhancing the intracellular labile iron pool (LIP) represents a powerful, yet untapp
37                         The reduction of the labile iron pool (LIP) suppressed the differentiation of
38 on taken up by the myocardium, intracellular labile iron pool (LIP) was imaged in FCM-treated mice an
39 arametric flow cytometry for quantitation of labile iron pool (LIP) was performed.
40 rotic cell death by moderating the amount of labile iron pool (LIP), but chronic use would cause seve
41 th TNF, this line fails to elevate levels of labile iron pool (LIP), critical for TNF-induced reactiv
42 , such as those that are bioavailable in the labile iron pool (LIP), react with thionitrite (SNO(-) )
43 portion of these species may constitute the "labile iron pool" (LIP) proposed in cellular Fe traffick
44 robe that enables longitudinal monitoring of labile iron pools (LIPs) in living animals.
45 ediated degradation of ferritin, increase in labile iron pool, ROS generation, and/or cell cycle arre
46 tein must scavenge iron from the endogenous, labile iron pool(s).
47 led from iron taken from the BIP-accessible, labile iron pool that is sampled also by ferritin and th
48 n of iron release required an intracellular "labile iron pool" that was rapidly depleted in the prese
49 al iron bound weakly to cellular ligands-the labile iron pool-to generate a response that preserves s
50  ferritin through ferritinophagy expands the labile iron pool, while activation of nuclear factor-ery
51      In addition, CK-666 does not impact the labile iron pool within cells nor does the inhibition of
52 scopy-based experiments allow the endogenous labile iron pool within growing cells to be detected wit
53  ions and is capable of detecting changes in labile iron pools within living cells with iron suppleme