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1 t express pan B-cell markers did not express Fas antigen.
2 malignant lymphoid cells is mediated by the Fas antigen.
3 ed normal transmembrane and death domains of Fas antigen.
4 ndent reduction in the surface expression of Fas antigen.
5 Bcl-2dim population expressed high levels of Fas antigen.
6 mediated apoptosis includes mutations in the Fas antigen.
7 analysis, all were found to be positive for Fas antigen.
8 expressing comparable levels of cell surface Fas antigen.
9 that was shown previously to associate with Fas antigen.
10 to regulate apoptotic signaling through the Fas antigen.
11 I MHC molecules, and increases expression of fas antigens.
15 munohistochemical analysis for expression of Fas antigen and CD31 (platelet-endothelial cell adhesion
18 ed: one in which the interaction between the Fas antigen and its ligand results in apoptosis, and ano
20 uding orosomucoid, amyloid, metallothionein, Fas antigen, and growth-related genes, including early g
21 g a monoclonal antibody directed against the Fas antigen, apoptosis was induced in freshly isolated m
22 three molecules regulating apoptosis, i.e., Fas antigen, Bax, and p53, at the genomic level in skin
23 to chemosensitivity and re-expression of the Fas antigen, but these cell lines did not regain the abi
24 oma cells (stably transfected to express the Fas antigen CD95, and denoted MCF7F) that lack detectabl
26 poptosis of CD4+ T cells and augmentation of Fas antigen (CD95, APO-1) expression in CD4+ and CD8+ T
29 ly, we demonstrate that mast cells from both Fas antigen-deficient mice and Nf1 +/- mice are resistan
30 background mutant mice which lack functional Fas antigen did not develop apoptosis in their Peyer's p
32 f1-deficient mast cells have reduced surface Fas antigen expression in response to kit-L and are resi
34 o decrease p21(ras) activity and up-regulate Fas antigen expression may limit the pathological accumu
35 reaction assays showed that the reduction of Fas antigen expression occurred at the level of transcri
36 ism of drug resistance showed no decrease of Fas antigen expression; however, the apoptotic response
37 g cause of gastric cancer, activation of the Fas antigen (Fas Ag) apoptotic pathway is responsible fo
38 s (PBMCs), but not H. pylori itself, induced Fas antigen (Fas Ag) expression, indicating a Fas-regula
39 cobacter infection up-regulated gastric cell Fas antigen (Fas Ag) mRNA and increased surface receptor
40 as used to identify intrarenal expression of Fas antigen, Fas ligand, granzyme B and perforin in eigh
44 ncing, we examined the cDNA structure of the Fas antigen in 54 bone marrow (BM) specimens obtained fr
46 ation normal T cell expressed and secreted), Fas antigen, Jun-B, c-Fos, macrophage colony-stimulating
47 ere located in the cytoplasmic region of the Fas antigen known to be involved in transduction of an a
49 hat increased B-cell Ao appears to be a FasL-Fas antigen-mediated process, but is not due to endotoxi
50 ment, there was significant up-regulation of Fas antigen mRNA and membrane localization of the recept
52 ns remains to be determined, we propose that Fas antigen mutations may contribute to the pathogenesis
53 ession and the functional status of the CD95/Fas antigen on primitive hematopoietic progenitors (PHPs
54 Fas mRNA was increased by 6 hours, whereas Fas antigen on the cell surface increased by 24 hours, w
55 ctivated or transformed cells expressing the Fas antigen on their surface are susceptible to killing
56 from patients with multiple myeloma, express Fas antigen on their surface, but do not undergo apoptos
58 atients display structural defects of either Fas antigen or ligand molecules, and although spontaneou
59 not observed with the p75 TNF receptor, the Fas antigen, or the p75 neurotrophin receptor, which are
63 s study, we show that mutations occur in the Fas antigen which may cause loss of function and contrib
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