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1 bited equally by either TNF(p60) or TNF(p80) mutein.
2 d by TNF and by p60 or p80 receptor-specific muteins.
3 major conformational changes in any of these muteins.
5 ities of chimeric interspecies and homologue muteins and epitope mapping of a monoclonal antibody (Mo
8 l model, predict that the properties of IL-2 mutein are a consequence of the reduction, of at least t
11 napse composed of membrane-tethered cytokine muteins bound to cell-surface cytokine receptors on tumo
12 ular variant of interleukin-6 (interleukin-6 mutein) but not with hepatocyte growth factor or lisofyl
14 increase in biological activity of the IL-15 mutein compared with the native molecule based on prolif
19 e NF-kappa B within 30 min, whereas TNF(p80) mutein, even at a 1000-fold excess, had no effect, sugge
25 sults in a product that fails to fold, while muteins H39A and H34A have activities very similar or id
26 ions, two survival-selective recombinant NGF muteins, i.e./7-84-103 and KKE/7-84-103, were generated.
27 tic excimer emission bands of pyrene-labeled muteins indicated stacking of the two pyrene rings in th
28 sis whereas wild-type TNF and TNFR2-specific mutein induce tubular cells to express proliferating cel
32 liary neurotrophic factor (CNTF), Axokine (a mutein of CNTF), leukemia inhibitory factor, basic fibro
33 opagate CAR(+) T cells, we developed a novel mutein of IL-21 bound to the cell surface of aAPC that r
35 The E13Y amino acid substitution of the IL13 mutein of the zetakine endows CTL transfectants with the
37 at neither the wild type nor any of the K152 muteins of MuLV RT are capable of forming stable ternary
39 e effects of shIL-4Ralpha and an IL-4 double mutein (R121D/Y124D, IL-4R antagonist) on IL-4- and IL-1
42 issue treated with wild-type TNF or specific muteins selective for TNFR1 (R1-TNF) or TNFR2 (R2-TNF).
45 P resistance patterns were unchanged for all muteins, suggesting no participation of K152 in ddNTP re
46 tudy was aimed at developing recombinant NGF muteins that did not support neuritogenesis while mainta
47 est a new option for HIV gene therapy; bcl-2 muteins that have noncleavable alterations surrounding t
48 ration of survival-selective recombinant NGF muteins that may represent novel pharmacologic lead agen
50 inding scFv and an IL13Ralpha2-binding IL-13 mutein to make a tandem CAR exodomain (TanCAR) and a CD2
54 F-mediated activation of NF-kappa B TNF(p60) mutein was also effective in cell killing, but the TNF(p
59 eted mutagenesis of human IL-2 to generate a mutein with approximately 3,000-fold in vitro selectivit
60 nt of its antiprotease activity because SLPI muteins, with significantly lower antiprotease activity,
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