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5 in ChlR1-depleted cells, but not in FANCJ(-/-) cells, when cells were treated with a triplex stabilizing compound benzoq
6 of BST2 was substantially inhibited by MLN4924 only when T cells were treated with alpha interferon (IFN-alpha) to induc
7 KSHV-infected-cell growth, primary effusion lymphoma (PEL) cells were treated with an iASPP inhibitor in the presence or
8 xplore the effects of EMD and TGF-beta1 on CTGF expression, cells were treated with and without TGF-beta inhibitor, and C
9 fect of the drug on MF stem cells (MF-SCs), splenic CD34(+) cells were treated with AZD1480 and transplanted into immunod
13 dditive or synergistic promoter activation when transfected cells were treated with combined stimuli.
19 Mice infected with 10(6) PbN-parasitized red blood cells were treated with either ET-1 or saline from 2 to 8 day
20 lation and inducibility of major human P450 enzymes, HepaRG cells were treated with either the WNT/beta-catenin signaling
21 treatment, with two distinct vesicle fractions present when cells were treated with epibromohydrin (EBH), a model epoxide
23 yonic stem cell-derived cardiomyocytes (hESC-CMs) and HepG2 cells were treated with glucose, and expression levels of NPs
24 Rat aortae and cultured rat aortic endothelial cells were treated with Hcy, BT extract, and theaflavin-3,3'-
28 resting cells myoferlin was bound to EHD2 protein and when cells were treated with IL-6, myoferlin dissociated from EHD2
29 MDA-MB-468 breast and HCT8 colorectal cancer cells were treated with inhibitors including LY294002, MK2206
31 more necrotic/apoptotic cells were found when these cancer cells were treated with IR-780 iodide with US irradiation.
36 key markers of pancreatic CSC was observed when MIA PaCa-2 cells were treated with MDB5 compared to GDC-0449.
37 king the MOBKL1B-NS5A interaction could not replicate after cells were treated with MOBKL1B siRNA.
40 Primary mouse hepatocytes (PMHs) and Huh7 cells were treated with palmitate or lysophosphatidylcholine
41 Human endothelial and smooth muscle cells were treated with pro-inflammatory cytokines with or wi
46 and MHC-II significantly increased when CML stem/progenitor cells were treated with the JAK1/2 inhibitor ruxolitinib (RUX
47 Upregulation of TLR expression was not evident when cells were treated with the neurokinin 1 receptor antagonist
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