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2 irion production from a chronically infected promonocytic cell line (U1) and in acutely infected mono
3 e activation of HIV in the latently infected promonocytic cell line (U1) and T-cell line (ACH-2) up-r
4 d induction of HIV expression in U1 cells, a promonocytic cell line chronically infected with HIV.
5 in monocytes, we transiently transfected the promonocytic cell line HL-60 with a chloramphenicol acet
6 Measurements of cyclin T1 mRNA levels in a promonocytic cell line suggested that regulation of cycl
7 for HIV-1 infectivity, clones from the U937 promonocytic cell line that express similar levels of CD
16 to plasma from diabetic patients, the human promonocytic cell line U937 exhibits a significant eleva
17 acetate (PMA)-induced differentiation of the promonocytic cell line U937 leads to persistent NF-kappa
18 al experiments revealed that exposure of the promonocytic cell line U937 to hypoxia resulted in incre
23 ivator of transcription-1 (Stat1) in a human promonocytic cell line, which was previously shown to be
26 st, phorbol ester-induced differentiation of promonocytic cell lines into macrophage-like cells produ
29 y based upon nonphysiological stimulation of promonocytic cell lines which may respond and process TA
33 R) function in cells expressing HIV-1, human promonocytic cells (U937) acutely or chronically infecte
34 st-transcriptional mechanism when human U937 promonocytic cells are stimulated to differentiate into
37 r restriction of M-tropic HIV-1 infection in promonocytic cells occurs at the fusion/entry level, tha
39 f phosphorylation in receptor function, U937 promonocytic cells were stably transfected to express th
40 ippled in their ability to replicate in U937 promonocytic cells, indicating that these sites are requ
41 f cervicovaginal epithelial cells and U1/HIV promonocytic cells, showed that multiple N-9 use can pro
50 P0 prevented HSV-1-induced disintegration of promonocytic leukemia (PML) nuclear bodies, an intracell
51 ze to punctate nuclear regions identified as promonocytic leukemia protein (PML) oncogenic domains (P
52 lar kinetics were observed with U-937 (human promonocytic leukemia) cells, used as a model for the bl
54 ort, we demonstrate that LPS-tolerized human promonocytic THP-1 cells develop cross-tolerance and no
55 we focused on the dynamic responses of human promonocytic THP-1 cells to lipopolysaccharide (LPS).
57 nomenon was observed in chronically infected promonocytic U1 cells differentiated to macrophage-like
58 ear pool of NF-kappaB (RelA and RelB) in the promonocytic U937 cell line using dominant-negative Ikap
59 omplement content, and incubated with either promonocytic U937 cells or normal human peripheral blood
60 lity of TNF-alpha to induce apoptosis in the promonocytic U937 cells, (ii) the discovery of a cross-t
61 increased expression of MHCII genes in human promonocytic U937 cells, which represent immature antige
64 erential TNF-alpha susceptibilities of human promonocytic U937 subclones, deficient in or overexpress
65 in-D(3)-induced differentiation of the human promonocytic U937cells, whereas ectopic SET expression i
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