ライフサイエンスコーパス: sodium arsenite

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 ular ROS induced by hypoxia/reoxygenation or sodium arsenite.

5 der conditions of severe stress induced with sodium arsenite.

6 en when exposed to chemical inducers such as sodium arsenite.

7 generated by exposing p53-knockdown HBECs to sodium arsenite (2.5 muM) for 16 weeks.

8 In this regard, we show that treatment with sodium arsenite, a known activator of p38 MAP kinases, a

9 duced heat-shock response can be mimicked by sodium arsenite, a nonthermal inducer of the heat-shock

10 We now report that sodium arsenite, a prototype for stressors fostering cyt

11 on of apoptosis by many chemicals, including sodium arsenite, a significant environmental contaminant

12 sed in the presence of etoposide (VP-16) and sodium arsenite, accompanied by equivalent decreases in

13 Treatment of cortical neurons with sodium arsenite activated p38 and JNK3 but not JNK1 or J

14 Insulin and sodium arsenite, an activator of the stress-activated pa

15 Sodium arsenite, an agent that induces oxidative stress,

16 ntly by transient treatment of cultures with sodium arsenite, an inducer of heat shock and oxidative

17 Here we have studied four stress agents: sodium arsenite, an oxidative agent; Gramicidin, eliciti

18 nts impaired ARE activation by the chemicals sodium arsenite and mercury chloride.

19 Sodium arsenite and osmotic shock both stimulated stress

20 eolin-1 to modulate the cellular response to sodium arsenite and thereby alter survival of the human

21 o temperature, pH, mitochondrial inhibitors, sodium arsenite, and many of the other stressors associa

22 the ars DNA promoter by phenylarsine oxide, sodium arsenite, and potassium antimonyl tartrate (in or

23 r exposure to noncytotoxic concentrations of sodium arsenite, and we confirmed some of these changes

24 Thus, sodium arsenite appears to promote SG formation and TDP-

25 Sodium arsenite (Ars) or hyperthermia (43 degrees C) ind

26 exposed to two inducers of cellular stress, sodium arsenite (As(III)), and vanadyl sulfate (V(IV)).

27 used to investigate the role of human BVR in sodium arsenite (As)-mediated induction of HO-1 and in c

28 xpressing cells appeared not to be unique to sodium arsenite, as wortmannin pretreatment also resulte

29 e involved in biogenesis of mitochondria for sodium arsenite (AsIII) and sodium arsenate (AsV) sensit

30 We report here that treatment of cells with sodium arsenite at the concentrations close to environme

31 was stimulated by treating erythrocytes with sodium arsenite but not by sodium arsenate (up to 1 mM).

32 Pretreatment of cells with 0.5 mM sodium arsenite (but not other activators of stress-acti

33 cells disassembled canonical SGs induced by sodium arsenite, but not those induced by hydrogen perox

34 The pro-oxidants sodium arsenite, cadmium chloride, and hydrogen peroxide

35 In LMH cells, sodium arsenite, cadmium, and heat shock, but not heme,

36 agents that induce oxidative stress, such as sodium arsenite, CCl4, lipopolysaccharide (LPS), or tumo

37 As a result, sodium arsenite completely abolished STAT activity-depen

38 omparable with that caused by calyculin A or sodium arsenite, compounds that cause a 2- to 3-fold inc

39 Arsenic trioxide and sodium arsenite did not directly modify or inhibit the a

40 adipocyte DNA damage with a high-fat diet or sodium arsenite exacerbated adipocyte senescence and met

41 ed drinking water with 0, 250 ppb, or 25 ppm sodium arsenite for 5 wk and then challenged intratrache

42 kb of the cHO-1 promoter region responded to sodium arsenite, H2O2, transition metals and 12-0-tetrad

43 by different exogenous stressors, including sodium arsenite, heat, and hippuristanol.

44 ve stress including ultraviolet irradiation, sodium arsenite, hyperoxia, and glutathione depletors.

45 s, we demonstrate that mice exposed to 0.01% sodium arsenite in drinking water develop hyperplasia of

46 of changes in mRNA stability in response to sodium arsenite in human fibroblasts.

47 However, the commonly used sodium arsenite in this solution has been omitted, makin

48 The sequence LPS/sodium arsenite increased the rate of endothelial cell a

49 Cells exposed to 10muM sodium arsenite increased the stability of HIPK1 and HIP

50 Furthermore, sodium arsenite induced Bim(EL) phosphorylation at Ser-6

51 Furthermore, sodium arsenite induced cortical neuron apoptosis.

52 ylatable S65A mutant of Bim(EL), potentiates sodium arsenite-induced apoptosis and by experiments sho

53 Here we report evidence that sodium arsenite-induced apoptosis in PC12 cells may be d

54 BP1) and colocalizes with G3BP1 in SGs under sodium arsenite-induced stress.

55 1N17) inhibits the hypoxia/reoxygenation and sodium arsenite-induced transcriptional activity of HSF-

56 Treatment with sodium arsenite induces stress granule formation in undi

57 ted that there are two regions important for sodium arsenite induction, one located between residues

58 t arsenicals, including arsenic trioxide and sodium arsenite, inhibited activation of the NLRP1, NLRP

59 Sodium arsenite is an environmental toxicant that causes

60 tudies were pursued with an oxidative agent (sodium arsenite), K-releasing agent (Gramicidin) and a m

61 ment of rat pheochromocytoma PC12 cells with sodium arsenite leads to enhanced expression of C/EBP-be

62 by heat shock treatment or after exposure to sodium arsenite, leads to a transient inhibition of Ikap

63 with gamma-irradiation, whereas exposure to sodium arsenite led to global increases in miRNA express

64 Thus, sodium arsenite may confer its cytotoxic effect partly t

65 th, relative to wild type, after exposure to sodium arsenite (NaAsO(2)).

66 ere, we studied the influence of heat shock, sodium arsenite (NaAsO2), cycloheximide (CHX) and Lipofe

67 and exposure to cadmium chloride (CdCl2) and sodium arsenite (NaAsO2).

68 Pregnant CD-1 mice were exposed to sodium arsenite [none (control), 10 ppb, or 42.5 ppm] in

69 luding heat shock treatment, and exposure to sodium arsenite or menadione, proved more toxic to those

70 milarly treatment of cells with puromycin or sodium arsenite, reagents that arrest translation, also

71 exate (MTX) and several metal salts, such as sodium arsenite, sodium arsenate, antimony potassium tar

72 n with actively translating ribosomes during sodium arsenite stress and discovered a set of transcrip

73 Pretreatment with sodium arsenite strongly inhibited IL-6-inducible STAT3

74 much more sensitive to the toxic effects of sodium arsenite than either untransfected parental cells

75 es of differentiated PC12 cells treated with sodium arsenite than in the soma or growth cones.

76 We examined herein the impact of sodium arsenite (the inorganic form of arsenic) on NF dy

77 After the addition of sodium arsenite to consume excess BrO-, yield is verifie

78 Moreover, sodium arsenite treatment may up-regulate expression of

79 ress stimuli (e.g. interleukin-3 withdrawal, sodium arsenite treatment, and peroxide treatment) is th

80 d p38 in cortical neuron apoptosis caused by sodium arsenite treatment.

81 ion, such binding was increased by cobalt or sodium arsenite treatment.

82 ly and reproducibly expressed in response to sodium arsenite treatment.

83 rrow toxicity, whereas the acute toxicity of sodium arsenite was equivalent in mrp(+/+) and mrp(-/-)

84 stimuli lipopolysaccharide [LPS] followed by sodium arsenite) was measured.

85 vincristine, doxorubicin, daunorubicin, and sodium arsenite were significantly greater in double kno

86 and Thr(287) allozymes, with K(m) values for sodium arsenite with the same allozymes of 11.8, 8.9, an