ライフサイエンスコーパス: TNFR-I

1 TNFR I/II-/- mice survived longer, dying between 15 and

2 TNFR-I (p55) function seems to be integral to the reject

3 TNFR-I possesses no intrinsic kinase activity, suggestin

4 TNFR-I-deficient BM was able to restore FDC organization

5 tance of DP thymocytes from TNF-alpha-/- and TNFR I-/-II-/- animals to cAMP agonist-mediated apoptosi

6 proteins between the human Fas receptor and TNFR I, each cysteine-rich domain of Fas was found to be

7 We investigated the role of LT-alpha and TNFR-I in the establishment of spleen FDC and GC structu

8 Both LT-alpha-/- and TNFR-I-/- mice lacked FDC clusters in LNs and spleen.

9 Interestingly, although both LT-alpha-/- and TNFR-I-/- mice that had been immunized with sheep red bl

10 Using neutralizing anti-TNFR-I and TNFR-II mAbs, we have now obtained evidence t

11 sociated proteins may provide a link between TNFR-I and ERK1/2 activation.

12 ls in the spleens of mice deficient for both TNFR I and TNFR II.

13 mice deficient in TNFR I (p55(-/-)) or both TNFR I and TNFR II (double knockout [DKO]) exhibited imp

14 LT-alpha-expressing BM-derived cells and by TNFR-I-expressing non-BM-derived cells.

15 RK1/2 activation are mediated exclusively by TNFR-I, not by TNFR-II.

16 Following high-dose IOE challenge, TNFR I/II-/- and TNF-alpha-depleted mice have an early i

17 FR-I (p55-/-), TNFR-II (p75-/-), or combined TNFR-I/TNFR-II deficiency (p55-/-p75-/-) and their wild-

18 MADD may couple TNFR-I with the ERK1/2 signaling pathway required for KS

19 Tumor necrosis factor receptor I-deficient (TNFR-I-/-) mice show similar absence of FDC clusters and

20 ressed the TNF-alpha receptor II, while Fas, TNFR-I, and CD27 expression were similar to CD49a(-) cel

21 In addition, macrophages from TNFR I/II double knockout mice were LPS tolerizable, and

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

23 including tumor necrosis factor receptor I (TNFR I), death receptor 3 and 4 (DR3 and DR4), and cytop

24 ell-surface receptors: TNF-alpha receptor-I (TNFR-I: p55) and TNF-alpha receptor-II (TNFR-II: p75).

25 Neutralizing anti-TNF receptor type I (TNFR-I; p55) Ab almost completely reversed TNF-alpha-ind

26 V from the liver and lung, mice deficient in TNFR I (p55(-/-)) or both TNFR I and TNFR II (double kno

27 Injection of interleukin 6 in TNFR-I-deficient animals 30 min before PH corrected the

28 Binding of AP-1 after PH was decreased in TNFR-I knockout mice compared with animals with the inta

29 Animals with gene-targeted deficiency in TNFR-I (p55-/-), TNFR-II (p75-/-), or combined TNFR-I/TN

30 , using primary Mphis from mice deficient in TNFR-I, TNFR-II, or both TNF-alpha receptors (TNFRs), we

31 In contrast, mesenteric LNs in TNFR-I-/- mice manifest grossly disturbed organization o

32 ma production in the spleens of IOE-infected TNFR I/II-/- and TNF-alpha-depleted mice was higher than

33 Interestingly, TNFR I CRD1 could partially substitute for the Fas CRD1.

34 ivating death domain protein (MADD), a novel TNFR-I-associated death domain protein.

35 a putative death domain similar to those of TNFR I and Fas.

36 a) or type I tumor necrosis factor receptor (TNFR-I), organized clusters of follicular dendritic cell

37 cking type I tumor necrosis factor receptor (TNFR-I).

38 en PGRN and tumor necrosis factor receptors (TNFR I/II) was reported and proposed to be a mechanism b

39 rmation of these structures does not require TNFR-I expression on BM-derived cells.

40 We conclude that TNFR I/II and TNF-alpha participate in Ehrlichia-induced

41 ptor I (TNFR I) and/or TNFR II, we show that TNFR I and TNFR II play redundant roles in down regulati

42 This indicates that TNFR-I expression on non-BM-derived cellular components

43 o intrinsic kinase activity, suggesting that TNFR-I-associated proteins may provide a link between TN

44 We therefore propose that the TNFR-I-ERK1/2 pathway plays a pivotal role in transmitti

45 lts indicate that TNF, signaling through the TNFR-I, can initiate liver regeneration and acts by acti

46 ever, the peptide had no effect on p55 TNFR (TNFR-I) expression.

47 In contrast, when TNFR-I-deficient mice were reconstituted with wild-type