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1 served mainly in tubular epithelial cells in CO-treated, but not air-exposed, kidney grafts at 3 hr a
2 rate that SFN reverses the effects of PMI in co-treated cells by reducing the accumulation of p62 in
3 s enhancer by nuclear proteins isolated from CO-treated cells, although HIF-1 protein levels were una
7 monstrate interesting activity profiles when co-treated in a panel of metal(II) cations in MIC assays
9 d upregulation of HIF-1alpha and VEGF in the CO-treated kidney grafts as early as 1 hr after reperfus
13 s to beta-amyloid (Abeta) peptides, we first co-treated primary cultured microglia with a tyrosine ph
15 otably, 10, 1 and 0.1 microM 3Me-H TRH, when co-treated with 500 microM Glu, protected fetal neurons
16 induction of hsp72 mRNA was blocked in cells co-treated with actinomycin D. hsp72 mRNA levels were af
18 g7 or Atg5 prolonged the survival of neurons co-treated with BDNF and rapamycin, suggesting that supp
20 a dramatic decrease in the survival of cells co-treated with Casodex and ATM inhibitor as compared wi
21 e in contrast to what we saw when cells were co-treated with cisplatin plus an EGFR tyrosine kinase i
24 so were studied in MG-63 cells that had been co-treated with either sterol and transforming growth fa
25 reactive oxygen species (ROS) scavenger, is co-treated with ETO, it inhibits an ETO-induced increase
26 17beta-estradiol (estrogen) for 1 h and then co-treated with glutamate, apoptotic death was significa
29 ted in response to thapsigargin if they were co-treated with PMA, while adherent cells secreted in re
32 deficient HL-60/MX2 cells and in HL-60 cells co-treated with the Top II catalytic inhibitor ICRF-193.
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