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1 lial migration could be blocked with soluble TNF receptor I.
2 neutralizing antibody and antibodies against TNF receptor I and -II blocked the induction of MMP-1 by
4 ha was abolished in macrophages deficient in TNF receptor I and II, Nlrp3, or ASC, whereas that induc
7 ncentrations of tumor necrosis factor (TNF), TNF receptors I and II (TNF-RI and TNF-RII), interleukin
8 matory (IL-10, IL-1 receptor antagonist, and TNF receptors I and II) cytokines in the blood after 21G
10 but not osteoproliferation, was dependent on TNF-receptor I and mediated by stromal tmTNF overexpress
14 fluorescent staining was used to investigate TNF receptor-I clustering at various time intervals afte
16 tal structures of TNF alpha and the TNF beta/TNF-receptor(I) complex and a model of an anti-TNF alpha
19 vo, signaling through the p55 subunit of the TNF receptor is essential for regulating hematopoiesis a
21 ical binding sites of tumor necrosis factor (TNF)-receptor(I) have been designed based on atomic feat
22 R-2, we determined whether signaling through TNF receptors is important for liver injury and hepatocy
24 icating that death signaling through Fas and TNF receptors is not essential for HA-induced thymocyte
26 ut mice lacking IL-1 receptor I (IL-1RI-/-), TNF receptor I (p55-/-), TNF receptor II (p75-/-), or bo
28 y, the protective effect of deletion of both TNF receptors is recapitulated in mice lacking only the
29 MP-12, TNF-alpha, IL-1alpha, IL-1beta, IL-6, TNF receptor I (RI), IL-1 RI, and IL-1 RII levels and th
31 , PKCepsilon facilitates the assembly of the TNF receptor-I signaling complex to trigger NF-kappaB ac
32 (IL-6), and their soluble receptors, soluble TNF receptor I (sTNF RI), sTNF RII, and sIL-6R and that
33 mice treated with a novel, soluble, dimeric TNF receptor I (sTNFRI) molecule capable of high-affinit
35 actor alpha (TNF-alpha) binds to its cognate TNF receptor I (TNF-RI) to stimulate inflammation via ac
36 RII) was localized in the cytoplasm, whereas TNF-receptor I (TNF-RI) was found in both cytoplasm and
39 ptor interacting protein kinase (RIPK1) from TNF receptor I (TNFR1) to form a caspase-8 activating co
40 cells were stained for CD3, CD4, CD8, CD28, TNF receptor I (TNFRI), and TNFRII, and analyzed by quan
42 ied (tumor necrosis factor alpha [TNFalpha], TNF receptor I [TNFRI], TNFRII, interleukin-1beta [IL-1b
43 h cell types expressed similar levels of the TNF-receptor I, whereas the Fas receptor was detected on