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2 ient in TNFR I (p55(-/-)) or both TNFR I and TNFR II (double knockout [DKO]) exhibited impaired viral
3 R I) and/or TNFR II, we show that TNFR I and TNFR II play redundant roles in down regulating the expa
6 ermined that the production of TNF-alpha and TNFR-II in response to AQARSAASKVKVSMKF preceded the pro
7 ay data, the protein levels of TNF-alpha and TNFR-II were increased following stimulation of RAW264.7
13 primary Mphis from mice deficient in TNFR-I, TNFR-II, or both TNF-alpha receptors (TNFRs), we determi
14 55-/-), TNFR-II (p75-/-), or combined TNFR-I/TNFR-II deficiency (p55-/-p75-/-) and their wild-type co
15 ceptor I (IL-1RI), IL-1RII, TNF receptor II (TNFR II), and IL-6 receptor as well as the level of proi
17 deficient for TNF receptor I (TNFR I) and/or TNFR II, we show that TNFR I and TNFR II play redundant
18 We propose that ligand binding to CD40 or TNFR II leads to the formation of a TRAF2/TANK complex,
19 r tumor necrosis factor receptor (TNFR)-I or TNFR-II have normal numbers of NK and NK/T cells, implyi
20 gene-targeted deficiency in TNFR-I (p55-/-), TNFR-II (p75-/-), or combined TNFR-I/TNFR-II deficiency
21 locking TNF in vivo by administering soluble TNFR II fusion protein (TNFRII:Fc) significantly reduced
24 lpha and one of its receptors, the p75 TNFR (TNFR-II), increasing 3.5- and 5.7-fold, respectively.
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