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1 ysate obtained from normal human mammary epithelial (HME-1) cells treated with variable doses (0-20 nM) of vitamin D for
2 The surviving fraction of MCF7 /: HER2-18 cells treated with (64)Cu-labeled trastuzumab (0.016-0.368 MB
10 ion and sequencing (RIP-seq) analyses of HuR in oral cancer cells treated with ionizing radiation (IR), determined that H
11 uR cleavage associated with active caspase-3 in oral cancer cells treated with ionizing radiation and chemotherapeutic dr
12 transcript heterogeneity in single Saccharomyces cerevisiae cells treated with and without salt stress to explore populat
14 emerges due to proliferation resembles that of low-density cells treated with a combination of IL-6/8.
15 revealed significantly more open clefts between endothelial cells treated with targeting, as opposed to non-targeting siR
18 , rather than cell size, is a key predictor of response for cells treated with high-frequency irreversible electroporatio
19 d compared with a database of gene expression profiles from cells treated with other bioactive small molecules.
21 In human colorectal carcinoma (HCT116) cells treated with H2O2, extracellular signal-regulated kinas
23 ralocorticoid receptor expression was also blunted in human cells treated with plasma from septic patients.
24 Ser-500 is found to undergo autophosphorylation in cells treated with ionomycin and is likely also targeted by P
25 es with UVB stimulated ROS production, which was reduced in cells treated with melatonin or its metabolites: 6-hydroxymel
27 Transmission electron micrographs (TEM) of infected cells treated with endocytosis inhibitors showed intact nucle
29 n increase in the optical force was also seen in macrophage cells treated with cytochalasin D, both with and without a su
30 Using a multiomics approach in mammalian cells treated with four types of mitochondrial stressors, we
33 Applying our approach to human melanoma cells treated with a panel of cancer therapeutics, we track d
34 strated the proliferative kinetics of BRAF-mutated melanoma cells treated with the BRAF inhibitor PLX4720 fall along a sp
36 Furthermore, human and mouse neuroblastoma cells treated with the amyloid-beta(1-42) peptide also showed
37 lecular biology techniques in both cultured neuroepithelial cells treated with a GCN5 inhibitor and forebrain tissue from
38 Zt6 protein on functional ribosomes, and in vitro assays of cells treated with recombinant Zt6 determined toxicity agains
39 novel Golgi-fragmenting agents, transcriptomic profiles of cells treated with brefeldin A, golgicide A, or monensin were
40 In contrast, cells in stationary growth phase or cells treated with a protonophore causing a decrease in cellu
42 ted by TET, significantly more PTX accumulated in A2780/PTX cells treated with PTX+TET/iRGD LPNs than either free drugs o
44 o closely resemble patterns and levels observed in the same cells treated with 20-200 pM EGF in vitro.
46 ephosphorylated in both Rheb-deficient CD4(+) T cells and T cells treated with rapamycin, suggesting mTORC1 signaling con
47 the induction of oxygen consumption rate observed in tubule cells treated with mPGC-1alpha serum.
48 erved in the tumor cells after OGT knockdown, whereas tumor cells treated with the O-GlcNAcase inhibitor showed an increa
50 Accumulation of ISGylated proteins in uninfected cells treated with dsDNA was prevented by expressing the HCMV
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