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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.
6 ities of chimeric interspecies and homologue muteins and epitope mapping of a monoclonal antibody (Mo
9 text for the therapeutic application of IL-2 muteins and highlight the importance of treatment timing
10 l model, predict that the properties of IL-2 mutein are a consequence of the reduction, of at least t
13 napse composed of membrane-tethered cytokine muteins bound to cell-surface cytokine receptors on tumo
14 ular variant of interleukin-6 (interleukin-6 mutein) but not with hepatocyte growth factor or lisofyl
15 to IL13Ralpha1 was sufficient to pacify IL13-mutein CAR T cells in the presence of IL13Ralpha1-overex
16 ppropriate selectivity while validating IL13-mutein CARs with improved selectivity for application to
18 increase in biological activity of the IL-15 mutein compared with the native molecule based on prolif
19 demonstrate that the cytokine mutant, IL-11 Mutein, competitively inhibits signalling in human cell
24 coli expressing murine decoy-resistant IL18 mutein (DR18) induced robust CD8(+) T and natural killer
27 acillus sp. MN chitosanase consisting of 167 muteins, enzymes that significantly differed in their su
28 e NF-kappa B within 30 min, whereas TNF(p80) mutein, even at a 1000-fold excess, had no effect, sugge
31 e activity of a CD8 T cell-preferential IL-2 mutein/Fc fusion protein with IL2 receptor beta linked t
36 sults in a product that fails to fold, while muteins H39A and H34A have activities very similar or id
37 A) to encode a half-life-extended human IL-2 mutein (HSA-IL2m) with mutations promoting reliance on I
38 ions, two survival-selective recombinant NGF muteins, i.e./7-84-103 and KKE/7-84-103, were generated.
39 ues engineered an Fc domain fused to a human mutein IL-2 (mIL-2-Fc) bearing mutations that confer pre
41 ntly produced IL-4 and IL-13 antagonist IL-4 mutein (IL-4M) on allergic sensitization and AIT outcome
42 ve ligation of TNFR2 with the TNFR2-specific mutein increased (pSer65-)4EBP1 expression in organ cult
43 tic excimer emission bands of pyrene-labeled muteins indicated stacking of the two pyrene rings in th
44 sis whereas wild-type TNF and TNFR2-specific mutein induce tubular cells to express proliferating cel
48 al for biotin binding, creating streptavidin muteins (M88 and M112) with novel disulfide-switchable b
49 get of rapamycin reduced both TNFR2-specific mutein-mediated phosphorylation of 4EBP1 and cell cycle
51 liary neurotrophic factor (CNTF), Axokine (a mutein of CNTF), leukemia inhibitory factor, basic fibro
52 opagate CAR(+) T cells, we developed a novel mutein of IL-21 bound to the cell surface of aAPC that r
54 The E13Y amino acid substitution of the IL13 mutein of the zetakine endows CTL transfectants with the
56 at neither the wild type nor any of the K152 muteins of MuLV RT are capable of forming stable ternary
60 e effects of shIL-4Ralpha and an IL-4 double mutein (R121D/Y124D, IL-4R antagonist) on IL-4- and IL-1
63 issue treated with wild-type TNF or specific muteins selective for TNFR1 (R1-TNF) or TNFR2 (R2-TNF).
65 virus (Flu) infection to determine how IL-2 mutein shapes T cell responses to respiratory virus infe
70 P resistance patterns were unchanged for all muteins, suggesting no participation of K152 in ddNTP re
71 e NSC, we generated 'agonist-only' Activin A muteins that activate ACVR1B but cannot form the NSC wit
73 tudy was aimed at developing recombinant NGF muteins that did not support neuritogenesis while mainta
74 est a new option for HIV gene therapy; bcl-2 muteins that have noncleavable alterations surrounding t
75 ration of survival-selective recombinant NGF muteins that may represent novel pharmacologic lead agen
77 inding scFv and an IL13Ralpha2-binding IL-13 mutein to make a tandem CAR exodomain (TanCAR) and a CD2
83 itumor effect, we generated a group of these muteins using phage display technology, in a previous wo
84 F-mediated activation of NF-kappa B TNF(p60) mutein was also effective in cell killing, but the TNF(p
92 eted mutagenesis of human IL-2 to generate a mutein with approximately 3,000-fold in vitro selectivit
93 The generation of IL-2 mutated variants (muteins) with changes in the affinity for different chai
94 nt of its antiprotease activity because SLPI muteins, with significantly lower antiprotease activity,