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1 purinic endonuclease 1 (Ape1) in response to sodium arsenite.
2 hort term treatment with either etoposide or sodium arsenite.
3 -resistant to carboplatin, methotrexate, and sodium arsenite.
4 der conditions of severe stress induced with sodium arsenite.
5 ular ROS induced by hypoxia/reoxygenation or sodium arsenite.
7 In this regard, we show that treatment with sodium arsenite, a known activator of p38 MAP kinases, a
8 duced heat-shock response can be mimicked by sodium arsenite, a nonthermal inducer of the heat-shock
10 on of apoptosis by many chemicals, including sodium arsenite, a significant environmental contaminant
11 sed in the presence of etoposide (VP-16) and sodium arsenite, accompanied by equivalent decreases in
15 ntly by transient treatment of cultures with sodium arsenite, an inducer of heat shock and oxidative
16 Here we have studied four stress agents: sodium arsenite, an oxidative agent; Gramicidin, eliciti
19 eolin-1 to modulate the cellular response to sodium arsenite and thereby alter survival of the human
20 o temperature, pH, mitochondrial inhibitors, sodium arsenite, and many of the other stressors associa
21 the ars DNA promoter by phenylarsine oxide, sodium arsenite, and potassium antimonyl tartrate (in or
22 r exposure to noncytotoxic concentrations of sodium arsenite, and we confirmed some of these changes
24 exposed to two inducers of cellular stress, sodium arsenite (As(III)), and vanadyl sulfate (V(IV)).
25 used to investigate the role of human BVR in sodium arsenite (As)-mediated induction of HO-1 and in c
26 xpressing cells appeared not to be unique to sodium arsenite, as wortmannin pretreatment also resulte
27 e involved in biogenesis of mitochondria for sodium arsenite (AsIII) and sodium arsenate (AsV) sensit
28 We report here that treatment of cells with sodium arsenite at the concentrations close to environme
29 was stimulated by treating erythrocytes with sodium arsenite but not by sodium arsenate (up to 1 mM).
31 cells disassembled canonical SGs induced by sodium arsenite, but not those induced by hydrogen perox
34 agents that induce oxidative stress, such as sodium arsenite, CCl4, lipopolysaccharide (LPS), or tumo
36 omparable with that caused by calyculin A or sodium arsenite, compounds that cause a 2- to 3-fold inc
38 adipocyte DNA damage with a high-fat diet or sodium arsenite exacerbated adipocyte senescence and met
39 ed drinking water with 0, 250 ppb, or 25 ppm sodium arsenite for 5 wk and then challenged intratrache
40 kb of the cHO-1 promoter region responded to sodium arsenite, H2O2, transition metals and 12-0-tetrad
42 ve stress including ultraviolet irradiation, sodium arsenite, hyperoxia, and glutathione depletors.
43 s, we demonstrate that mice exposed to 0.01% sodium arsenite in drinking water develop hyperplasia of
50 ylatable S65A mutant of Bim(EL), potentiates sodium arsenite-induced apoptosis and by experiments sho
52 1N17) inhibits the hypoxia/reoxygenation and sodium arsenite-induced transcriptional activity of HSF-
54 ted that there are two regions important for sodium arsenite induction, one located between residues
55 t arsenicals, including arsenic trioxide and sodium arsenite, inhibited activation of the NLRP1, NLRP
57 tudies were pursued with an oxidative agent (sodium arsenite), K-releasing agent (Gramicidin) and a m
58 ment of rat pheochromocytoma PC12 cells with sodium arsenite leads to enhanced expression of C/EBP-be
59 by heat shock treatment or after exposure to sodium arsenite, leads to a transient inhibition of Ikap
60 with gamma-irradiation, whereas exposure to sodium arsenite led to global increases in miRNA express
63 ere, we studied the influence of heat shock, sodium arsenite (NaAsO2), cycloheximide (CHX) and Lipofe
66 luding heat shock treatment, and exposure to sodium arsenite or menadione, proved more toxic to those
67 milarly treatment of cells with puromycin or sodium arsenite, reagents that arrest translation, also
68 exate (MTX) and several metal salts, such as sodium arsenite, sodium arsenate, antimony potassium tar
70 much more sensitive to the toxic effects of sodium arsenite than either untransfected parental cells
75 ress stimuli (e.g. interleukin-3 withdrawal, sodium arsenite treatment, and peroxide treatment) is th
79 rrow toxicity, whereas the acute toxicity of sodium arsenite was equivalent in mrp(+/+) and mrp(-/-)
81 vincristine, doxorubicin, daunorubicin, and sodium arsenite were significantly greater in double kno
82 and Thr(287) allozymes, with K(m) values for sodium arsenite with the same allozymes of 11.8, 8.9, an
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