ライフサイエンスコーパス: TNF receptor I

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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

3 protein involved in signal transduction from TNF receptor I and II and related receptors.

4 ha was abolished in macrophages deficient in TNF receptor I and II, Nlrp3, or ASC, whereas that induc

5 Topical administration of soluble TNF receptor I and IL-1 receptor antagonist, which abrog

6 steps regulating this process, clustering of TNF receptor-I and caspase-3 activation.

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

9 mains of both Fas and tumor necrosis factor (TNF) receptors I and II.

10 We have found that soluble TNF receptor-I attenuated LPS inhibition of phagocytosis

11 MyD88, tumor necrosis factor (TNF)-alpha, or TNF receptor I but not interleukin-6 or -12p40.

12 fluorescent staining was used to investigate TNF receptor-I clustering at various time intervals afte

13 UVB or TNF-alpha promoted TNF-receptor-I clustering, a process inhibited by the tr

14 tal structures of TNF alpha and the TNF beta/TNF-receptor(I) complex and a model of an anti-TNF alpha

15 is mediated through one or both forms of the TNF receptor is controversial.

16 vo, signaling through the p55 subunit of the TNF receptor is essential for regulating hematopoiesis a

17 cluding normal bacterial flora, and requires TNF receptor I function.

18 ical binding sites of tumor necrosis factor (TNF)-receptor(I) have been designed based on atomic feat

19 R-2, we determined whether signaling through TNF receptors is important for liver injury and hepatocy

20 First, TNF acting through TNF receptor is involved in the development/maturation o

21 icating that death signaling through Fas and TNF receptors is not essential for HA-induced thymocyte

22 expression of Fas or tumor necrosis factor (TNF) receptors is not required for CD8-mediated GVL.

23 ut mice lacking IL-1 receptor I (IL-1RI-/-), TNF receptor I (p55-/-), TNF receptor II (p75-/-), or bo

24 ble TNF, recombinant methionyl human soluble TNF receptor I (p55-TNFRI), or adalimumab.

25 y, the protective effect of deletion of both TNF receptors is recapitulated in mice lacking only the

26 MP-12, TNF-alpha, IL-1alpha, IL-1beta, IL-6, TNF receptor I (RI), IL-1 RI, and IL-1 RII levels and th

27 The other components of the TNF receptor I signaling cascade were not altered, where

28 , PKCepsilon facilitates the assembly of the TNF receptor-I signaling complex to trigger NF-kappaB ac

29 (IL-6), and their soluble receptors, soluble TNF receptor I (sTNF RI), sTNF RII, and sIL-6R and that

30 mice treated with a novel, soluble, dimeric TNF receptor I (sTNFRI) molecule capable of high-affinit

31 Fas and TNF receptor I (TNF-RI) share homology at their cytoplas

32 actor alpha (TNF-alpha) binds to its cognate TNF receptor I (TNF-RI) to stimulate inflammation via ac

33 RII) was localized in the cytoplasm, whereas TNF-receptor I (TNF-RI) was found in both cytoplasm and

34 Using mice deficient for TNF receptor I (TNFR I) and/or TNFR II, we show that TNF

35 Male tumor necrosis factor (Tnf) receptor I (Tnfr-/-) mice and C57BLJ wild type (WT)

36 ptor interacting protein kinase (RIPK1) from TNF receptor I (TNFR1) to form a caspase-8 activating co

37 cells were stained for CD3, CD4, CD8, CD28, TNF receptor I (TNFRI), and TNFRII, and analyzed by quan

38 TNF-receptor I (TNFRI) mutant mice were protected from i

39 ied (tumor necrosis factor alpha [TNFalpha], TNF receptor I [TNFRI], TNFRII, interleukin-1beta [IL-1b

40 h cell types expressed similar levels of the TNF-receptor I, whereas the Fas receptor was detected on

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