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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.
12     Of the 48 BM specimens which did express Fas antigen, 5 (10%) displayed point mutations.
13                                Engagement of Fas antigen, a potent effector of apoptosis, activates c
14            Normal expression of cell surface Fas antigen accompanied by defects in late activation th
15 munohistochemical analysis for expression of Fas antigen and CD31 (platelet-endothelial cell adhesion
16 at penetrate the cornea coexpressed both the Fas antigen and CD31.
17       IAV increased neutrophil expression of Fas antigen and Fas ligand, and it also increased releas
18 ed: one in which the interaction between the Fas antigen and its ligand results in apoptosis, and ano
19              Expression levels of cytokines, Fas antigen, and Fas ligand (TaqMan quantitation) in PBM
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
25 iffusely express Fas ligand (CD95L), but not Fas antigen (CD95).
26 poptosis of CD4+ T cells and augmentation of Fas antigen (CD95, APO-1) expression in CD4+ and CD8+ T
27                                          The Fas antigen (CD95, APO-1) is a transmembrane cell surfac
28                                              Fas antigen-deficient (lpr) mice or C57BL/6 wild-type mi
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
31         Oncogenic p21(ras) decreases surface Fas antigen expression and renders fibroblasts resistant
32 f1-deficient mast cells have reduced surface Fas antigen expression in response to kit-L and are resi
33                      Genetic loss of surface Fas antigen expression leads to reduced apoptosis of mye
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
41           To study the molecular fate of the Fas antigen following receptor activation, a monoclonal
42            Loss of function mutations in the Fas antigen have been associated with congenital autoimm
43                             Mutations in the Fas antigen have not been previously described in cancer
44 ncing, we examined the cDNA structure of the Fas antigen in 54 bone marrow (BM) specimens obtained fr
45                             The mechanism of Fas antigen-induced hepatocyte apoptosis was investigate
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
48                          Early in infection, Fas antigen-mediated apoptosis depletes parietal and chi
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
51 s (11%) did not express detectable levels of Fas antigen mRNA.
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
57 carcinoma cell lines heterogeneously express Fas antigen on their surface.
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
60 -7 (Mch-3alpha) were rapidly processed after Fas antigen stimulation.
61 (TNF) receptor shares with the related APO-1/Fas antigen the ability to initiate apoptosis.
62 induced TNF-alpha IFN-gamma secretion and of Fas antigen upregulation.
63 s study, we show that mutations occur in the Fas antigen which may cause loss of function and contrib
64  cell lysates to identify different forms of Fas antigens without immunoprecipitation.

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