ライフサイエンスコーパス: TNFR

1 TNFR expression on mononuclear cells from the dermis and

2 TNFR KO mice showed higher baseline SWS delta power.

3 TNFR levels were unrelated to baseline free TNFalpha lev

4 TNFR superfamily (TNFRSF) members have important immunor

5 TNFR superfamily (TNFRSF)4 (OX40, CD134) and TNFRSF25 ar

6 TNFR-associated death domain protein (TRADD) is a key ef

7 TNFR/TNF superfamily members can control diverse aspects

8 The 55-kDa type 1 TNFR (TNFR1), the key receptor for TNF signaling, is rel

9 th baseline levels of plasma TNF receptor-1 (TNFR-1), TNFR-2, and kidney injury molecule-1 (KIM-1) fo

10 ation (such as MCP-1, suPAR, TNF receptor-1 [TNFR-1], and TNFR-2) may identify children with CKD at r

11 ne levels of plasma TNF receptor-1 (TNFR-1), TNFR-2, and kidney injury molecule-1 (KIM-1) for the out

12 Higher plasma KIM-1, TNFR-1, and TNFR-2 are independently associated with CKD

13 le adjustment, children with a plasma KIM-1, TNFR-1, or TNFR-2 concentration in the highest quartile

14 KIM-1, TNFR-1, TNFR-2, and YKL-40 were associated with rate of

15 Higher plasma levels of KIM-1, TNFR-1, TNFR-2, MCP-1, suPAR, and YKL-40 were associated

16 Higher concentrations of KIM-1, TNFR-1, TNFR-2, MCP-1, suPAR, and YKL-40 were each assoc

17 r injury, inflammation, and fibrosis (KIM-1, TNFR-1, TNFR-2, MCP-1, suPAR, and YKL-40).

18 accounting for competing biomarkers, KIM-1, TNFR-2, and YKL-40 remained associated with progression

19 ings validate previous literature on TNFR-1, TNFR-2, and KIM-1 in patients with prevalent CKD and pro

20 In conclusion, TNFR-1, TNFR-2, and KIM-1 independently associated with higher r

21 Associations between doubling in TNFR-1, TNFR-2, and KIM-1 levels and risk of the renal outcomes

22 t baseline, median concentrations of TNFR-1, TNFR-2, and KIM-1 were roughly two-fold higher in the ad

23 KIM-1, TNFR-1, TNFR-2, and YKL-40 were associated with rate of eGFR dec

24 Higher plasma levels of KIM-1, TNFR-1, TNFR-2, MCP-1, suPAR, and YKL-40 were associated with in

25 Higher concentrations of KIM-1, TNFR-1, TNFR-2, MCP-1, suPAR, and YKL-40 were each associated wi

26 , inflammation, and fibrosis (KIM-1, TNFR-1, TNFR-2, MCP-1, suPAR, and YKL-40).

27 iRNAs like miR-155-5p modulate TLR-, IL-1R-, TNFR-, and IFNAR-mediated signaling pathways upstream of

28 h domain adaptor molecule (FADD), caspase-8, TNFR-associated factor 2 (TRAF2), and receptor-interacti

29 expressing in B lymphocytes both BCL-2 and a TNFR-associated factor 2 (TRAF2) mutant lacking the real

30 9-producing CD4(+) T-helper (TH9) cells in a TNFR-associated factor 6 (TRAF6)- and NF-kappaB-dependen

31 CD27 is a TNFR family member expressed on T cells, and its ligand,

32 -FMK also induced Rip1-phosphorylation via a TNFR-independent mechanism.

33 hrough its interactions with tubulin, actin, TNFR-associated factor-3 (Traf3), IL-13R1, and DISC1.

34 signaling complex that contained the adapter TNFR-associated factor 2 as well as PKB and its upstream

35 The signaling adaptor TNFR-associated factor 1 (TRAF1) is specifically lost fr

36 Rs not only have implications for additional TNFR family members, but also provide potential targets

37 une mediators/regulators linked to TNF-alpha/TNFR signaling, nuclear factor kappa-B (NF-kappaB) activ

38 lant rejection that is exclusively TNF-alpha/TNFR-dependent.

39 Two counterregulatory molecules, TNF-alphaR (TNFR) 1 and TNFR2, modulate the pathological effects of

40 quartile (a 4-fold higher risk for KIM-1 and TNFR-1 and a 2-fold higher risk for TNFR-2).

41 itment of receptor interacting protein 1 and TNFR-associated factor 2 to the DR3 signaling complex an

42 sma KIM-1, YKL-40, MCP-1, suPAR, TNFR-1, and TNFR-2 are associated with GFR decline in children with

43 Higher plasma KIM-1, TNFR-1, and TNFR-2 are independently associated with CKD progression

44 TBK1, TGF-beta-activated kinase (TAK) 1, and TNFR-associated factor 6, whereas not affecting p65-indu

45 s MCP-1, suPAR, TNF receptor-1 [TNFR-1], and TNFR-2) may identify children with CKD at risk for GFR d

46 IKKepsilon, TNFR-associated factor 2, and TNFR-associated factor 5 were also required to mediate t

47 in global sleep architecture in C57BL/6J and TNFR KO mice.

48 ted with TNF-alpha neutralizing antibody and TNFR KO mice showed increased EEG SWS activity.

49 ed on TNF production by BM-derived cells and TNFR expression by radioresistant IECs.

50 the population of highly injected cells, and TNFR-deficient mice displayed enhanced susceptibility to

51 sis factor receptors (TNFRs): Fas, FasL, and TNFR superfamily member 1B.

52 naling through its interaction with NEMO and TNFR-associated factor 2.

53 sponsible for its association with OX40, and TNFR-associated factor 2 (TRAF2) bridged these two prote

54 ctivated kinase 1 (TAK1) phosphorylation and TNFR-associated factor (TRAF) 6 ubiquitination in BMMCs

55 ereas MyD88, Toll/IL-1R adaptor protein, and TNFR-alpha-associated factor 6 recruitments to TLR2 were

56 -family adapter proteins involved in TLR and TNFR pathways.

57 Our results reveal that a prototypic TLR and TNFR signaling pathway is used by a killer cell Ig-like

58 se, IRAK1, TLR1, TLR4, TLR6, TLR8, TLR9, and TNFR-associated factor 6) were downregulated, whereas an

59 ptors, including those of the Notch, Wnt and TNFR/IKK/NF-kappaB pathways, and discuss the potential r

60 II, but not the interaction between PGRN and TNFRs.

61 l or functional interaction between PGRN and TNFRs.

62 ow demonstrate that different agonistic anti-TNFR antibodies have specific requirements for FcgammaRI

63 optimal biological effects of agonistic anti-TNFR antibodies.

64 ign of more potent antitumor agonistic, anti-TNFR therapies, the underlying mechanism has remained ob

65 domain-containing adaptor inducing IFN-beta/ TNFR-associated factor 3 pathway was highly upregulated

66 However, cell death protection through both TNFR was mediated through the Bcl-2/Bcl-xL pathway.

67 l can be mediated independently through both TNFR.

68 mitochondrial depolarization is mediated by TNFR-associated factor-1 (TRAF-1) and TRAF-2 degradation

69 LR families, whose signals are transduced by TNFR-associated factor (TRAF) molecules.

70 mice expressing the mitochondrial chaperone TNFR-associated protein 1 (TRAP1) in the prostate develo

71 he expression of the mitochondrial chaperone TNFR-associated protein-1 (TRAP1) in cancer.

72 Using an established system of chimeric TNFRs and novel ligand variants mimicking the bioactivit

73 sion, elevated concentrations of circulating TNFRs in patients with type 2 diabetes at baseline are v

74 In conclusion, TNFR-1, TNFR-2, and KIM-1 independently associated with

75 We identified a conserved TNFR-associated factor 6 (TRAF6) binding motif, which wa

76 n this study, we show that the costimulatory TNFR CD27 provides a dual trigger that can enhance survi

77 The costimulatory TNFR family member GITR can provide important survival s

78 treatment with the cTfRMAb-GDNF and cTfRMAb-TNFR fusion proteins caused a significant 54%, 69% and 3

79 or (d) the combined cTfRMAb-GDNF and cTfRMAb-TNFR fusion proteins, following a 1-h reversible middle

80 eins are designated cTfRMAb-GDNF and cTfRMAb-TNFR, respectively.

81 nflammatory therapies based on soluble decoy TNFRs.

82 tions in vitro to limit caspase-8-dependent, TNFR-induced apoptosis, and animals lacking RIPK1, RIPK3

83 erated potent agonists against two different TNFR superfamily receptors and mouse tumor model studies

84 with progression of diabetic kidney disease; TNFR-2 had the highest risk (adjusted hazard ratio, 1.61

85 k of progression of diabetic kidney disease; TNFR-2 had the highest risk after accounting for the oth

86 velopment and highlight the role of distinct TNFRs in initial and terminal differentiation stages in

87 diate p75(NTR) signaling are trimeric (i.e., TNFR-associated factor 6 or TRAF6).

88 h receptors nor the classical MAVS effectors TNFR-associated factor-2, IRF-3/7, or IFN-beta but the p

89 nsistent with the hypothesis that epithelial TNFR signaling participates in mucosal healing.

90 These encouraging data establish TNFRs as important targets for enhancing tumor-specific

91 perfamily member 15 (TL1A) is the ligand for TNFR superfamily (TNFRSF)25.

92 ization and clustering is a prerequisite for TNFR intracellular signaling, and as m4-1BBL can only re

93 IM-1 and TNFR-1 and a 2-fold higher risk for TNFR-2).

94 s were incubated with conditioned media from TNFR-costimulated T lymphocytes, and type I collagen exp

95 ive and argue for the use of next-generation TNFR-selective TNF therapeutics as an effective approach

96 atment with BBB penetrating IgG-GDNF and IgG-TNFR fusion proteins enhances the therapeutic effect of

97 ese effects are mediated through the type II TNFR (TNFR2).

98 IKKepsilon, TNFR-associated factor 2, and TNFR-associated factor 5 w

99 ies of antibodies targeting immunoregulatory TNFRs expressed by T cells.

100 mation over 3 days; hgd40 reduced colitis in TNFR double-knockout mice.

101 Associations between doubling in TNFR-1, TNFR-2, and KIM-1 levels and risk of the renal o

102 Further, in TNFR(-/-) mice, neutrophils accumulated normally in resp

103 d SCN activation in control mice, but not in TNFR-1 mutants.

104 r 2 (TRAF2), suggesting a regulatory role in TNFR signaling.

105 decreased in C57BL/6J, and was unaffected in TNFR KO mice as well as in C57BL/6J mice exposed to SF b

106 Glucocorticoid-induced TNFR (Gitr) and Ox40, two members of the TNFR superfamil

107 n, CTLA-4 exon 2, and glucocorticoid-induced TNFR exon 5, were phenotypically unstable, and exhibited

108 Glucocorticoid-induced TNFR family related gene (GITR) is a member of the TNFR

109 t by upregulating the glucocorticoid-induced TNFR family-related protein (GITR) and increasing GITR s

110 Glucocorticoid-induced TNFR family-related protein (GITR)-mediated activation o

111 n has shown that anti-glucocorticoid-induced TNFR family-related protein agonistic Ab DTA-1 (rat or m

112 receptor binding and glucocorticoid-induced TNFR family-related protein-induced T cell agonistic pro

113 h a stimulatory Ab to glucocorticoid-induced TNFR family-related receptor (GITR) has previously been

114 icant upregulation of glucocorticoid-induced TNFR family-related receptor on conventional T cells dur

115 a their expression of glucocorticoid-induced TNFR ligand.

116 her, T cell-intrinsic glucocorticoid-induced TNFR-related protein (GITR) contributes to 4-1BB express

117 Glucocorticoid-induced TNFR-related protein (GITR) is a costimulatory molecule

118 se targeting OX40 and glucocorticoid-induced TNFR-related protein (GITR).

119 levated expression of glucocorticoid-induced TNFR-related protein (GITR).

120 es targeting the TNFR glucocorticoid-induced TNFR-related protein (GITR; TNFRSF18; CD357) expressed o

121 CD27, TNFR2 p75, and glucocorticoid-induced TNFR-related protein compared with transferred CD28(+/+)

122 Agonistic antibodies to apoptosis-inducing TNFRs, such as death receptor 5 (DR5), although displayi

123 We investigated TNFR expression in clinical samples and function in shor

124 ifs found in the cytoplasmic domains of many TNFR family members and their adaptor proteins may serve

125 wever, PG102 stimulated normal CD40-mediated TNFR-associated factor (TRAF)2 and TRAF3 degradation.

126 6J and in TNF-alpha double receptor KO mice (TNFR KO).

127 vivo, and treatment with the small molecule TNFR inhibitor R-7050 partially protected hyperoxaluric

128 Rs extended to an antibody targeting the non-TNFR receptor CTLA-4 (CD152) that acts as a negative reg

129 nvolves hemopoietic cross-talk, and numerous TNFR superfamily members have been implicated in this pr

130 in systemic inflammation, whereas absence of TNFR or Fas signaling protected mice from CD4(+) T cell-

131 tly can augment the anti-tumor activities of TNFR antibodies by enhancing their agonistic activities

132 nsequently, generating effective agonists of TNFR superfamily receptors is challenging.

133 and themselves, and regulate the assembly of TNFR signalling complexes.

134 Furthermore, therapeutic blockade of TNFR might delay progressive forms of nephrocalcinosis i

135 At baseline, median concentrations of TNFR-1, TNFR-2, and KIM-1 were roughly two-fold higher i

136 of osteoclastogenesis and for degradation of TNFR-associated factor 6 in osteoclast precursors.

137 usly found that T cell-intrinsic deletion of TNFR-associated factor (TRAF) 6 (TRAF6DeltaT) in mice re

138 he signal transduction network downstream of TNFR and upstream of IKK, and depends on the level of th

139 Expression of TNFR and IL-6 in the dermis was reversible in a patient

140 ogenic activities by retaining expression of TNFR-1 and -2 and VEGF receptor 2 in ECs.

141 CHQ elevated expression of TNFR-associated factor 6, a common intermediate in IL-1R

142 R2, we demonstrate differential functions of TNFR in human monocyte-derived and blood CD1c(+) DC.

143 L-1R-associated kinase 1, but independent of TNFR-associated factor 6.

144 Inhibition of TNFR signaling prevented the induced expression of the c

145 a suggest that iRhom2-mediated inhibition of TNFR signaling protects against liver fibrosis.

146 indings demonstrate that PGRN is a ligand of TNFR, an antagonist of TNFalpha signaling, and plays a c

147 ovision of costimulation through ligation of TNFR family members, such as OX40 (CD134), provides esse

148 It also suggests that TRAF6, a mediator of TNFR and TLR signaling, may be a common signaling interm

149 uce the freely available cytoplasmic pool of TNFR-associated factor (TRAF)2 and cellular inhibitors o

150 In this study, we examined the role of TNFR-associated factor (TRAF)4 in IL-17 signaling and Th

151 ] is an essential kinase linking a subset of TNFR family members to the noncanonical NF-kappaB pathwa

152 40 and mediates K63-linked ubiquitination of TNFR-associated factor3 (TRAF3).

153 that are best known as signaling adapters of TNFRs.

154 Concentrations of TNFRs moderately associated with death unrelated to ESRD

155 While the extracellular domains of TNFRs form trimeric complexes with their ligands and the

156 ovide evidence for a stepwise involvement of TNFRs in mTEC development, with CD40 upregulation induce

157 om2 in promoting ADAM17-mediated shedding of TNFRs in hepatic stellate cells, which reduces TNFR sign

158 ecruitment of PKB and PI3K were dependent on TNFR-associated factor 2 and on translocation of OX40 in

159 ese findings validate previous literature on TNFR-1, TNFR-2, and KIM-1 in patients with prevalent CKD

160 We now show that one TNFR family member, OX40 (CD134), after ligation by OX40

161 iR-146a targets IL-1R-associated kinase 1 or TNFR-associated factor 6, suggesting the regulatory effe

162 nt, children with a plasma KIM-1, TNFR-1, or TNFR-2 concentration in the highest quartile were at sig

163 iated immune cell responses in TNF-alpha- or TNFR-deficient mice.

164 e received TNFR 1 (p55) knockout (KO) and/or TNFR 2 (p75) KO donor T cells.

165 n of engineered antibodies to OX40 and other TNFR with improved anti-tumor activity.

166 yer in controlling the availability of other TNFR family members.

167 Analysis of other TNFR sequences suggests proline-containing sequences as

168 In contrast to other TNFR agonists, such as anti-4-1BB, which can cause immun

169 Similar to other TNFR ligands, CD70 has been shown to initiate intracellu

170 , raising the possibility that aberrant PGRN-TNFR interactions underlie the molecular basis for neuro

171 sative agent of smallpox, is the most potent TNFR of those tested here including hTNFR2.

172 with the soluble recombinant fusion protein TNFR:Fc slowed disease progression in UmodC147W/+ mice b

173 ectrometry for the LTbetaR signaling protein TNFR-associated factor 3 (TRAF3).

174 The cytoplasmic adaptor proteins TNFR-associated factor (TRAF)3 and TRAF6 are important m

175 sequently, in the absence of c-IAP proteins, TNFR-mediated activation of NF-kappaB and MAPK pathways

176 eby limiting crosstalk between ITAM and RANK/TNFR signaling and allowing fine tuning of osteoclastoge

177 cells in a signal 3 manner, F1 mice received TNFR 1 (p55) knockout (KO) and/or TNFR 2 (p75) KO donor

178 ctivated CD4(+) T cells engaged its receptor TNFR on MPs, leading to pro-IL-1beta synthesis.

179 peripheral glia, and the TNF-alpha receptor (TNFR), Wengen, is expressed in motoneurons.

180 ptor (TLR) and TNF-family cytokine receptor (TNFR) signaling pathways.

181 deletion of tumor necrosis factor receptor (TNFR) 1 and TNFR2 (TNFR double knockouts); some mice wer

182 ction of the tumor necrosis factor receptor (TNFR) CD27 with its ligand CD70 is an emerging target to

183 the type II tumor necrosis factor receptor (TNFR) decoy receptor.

184 that target tumor necrosis factor receptor (TNFR) family members have shown dependence on expression

185 nal from the tumor necrosis factor receptor (TNFR) family molecule OX40 (CD134), which is induced on

186 mbers of the tumor necrosis factor receptor (TNFR) family with agonist Abs enhances T cell function,

187 ruses encode tumor necrosis factor receptor (TNFR) homologs or viral TNFR (vTNFR).

188 nging to the tumor necrosis factor receptor (TNFR) superfamily are emerging as promising cancer immun

189 sponses, the tumor necrosis factor receptor (TNFR) superfamily members have emerged as attractive tar

190 a member of tumour necrosis factor receptor (TNFR) superfamily, has a pivotal role in B-cell-mediated

191 mber of the tumour necrosis factor receptor (TNFR) superfamily, has the capacity to cause extensive a

192 ember of the tumor necrosis factor receptor (TNFR) superfamily, is expressed on antigen-presenting ce

193 ember of the tumor necrosis factor receptor (TNFR) superfamily, whose members undergo trimeric oligom

194 eptor in the tumor necrosis factor receptor (TNFR) superfamily.

195 tor (TLR)-2, tumor necrosis factor receptor (TNFR)-1 and closely related NOD1, all of which share com

196 Ablation of tumour necrosis factor receptor (TNFR)-1/-2, Myeloid Differentiation primary response gen

197 Tumor necrosis factor receptor (TNFR)-associated factor 2 (TRAF2) is a pivotal intracell

198 pter protein tumor necrosis factor receptor (TNFR)-associated factor 3 (TRAF3) is both modified by an

199 Tumor necrosis factor receptor (TNFR)-associated factor 6 (TRAF6) is an adapter protein

200 Tumor necrosis factor receptor (TNFR)-associated factor 6 (TRAF6) is an important adapto

201 Tumor necrosis factor receptor (TNFR)-associated factors (TRAFs) form a family of protei

202 ogy with the tumor-necrosis-factor receptor (TNFR)-associated factors TRAF2 and TRAF3.

203 coid-induced tumor necrosis factor receptor (TNFR)-related protein (GITR) elicits antitumor activity

204 actor in the tumor necrosis factor-receptor (TNFR) and Toll-like receptor (TLR) pathways.

205 urther analysis, antibodies to TNF receptor (TNFR) 1 or 2 were applied, or CSD was monitored in TNFR1

206 Selective inhibition of TNF receptor (TNFR) 1 signaling holds the potential to greatly reduce

207 use of the differential use of TNF receptor (TNFR) family costimulatory receptors.

208 Individual TNF receptor (TNFR) signaling in RBR was evaluated in BM-EPCs from WT,

209 ptosis, processes that involve TNF receptor (TNFR) signaling.

210 costimulatory molecules in the TNF receptor (TNFR) superfamily are viewed as a major source of this s

211 Agonistic anti-TNF receptor (TNFR) superfamily member antibodies are a class of promi

212 LMP1 functionally mimics TNF receptor (TNFR) superfamily member CD40, but LMP1 signals and down

213 ath receptors, a subset of the TNF receptor (TNFR) superfamily.

214 ingly suppressed expression of TNF receptor (TNFR)-1 and -2, decreased TNF-alpha-induced phosphorylat

215 o investigate the influence of TNF receptor (TNFR)-costimulated lymphocytes on collagen expression in

216 of the tumor-necrosis factor (TNF) receptor (TNFR)-associated factor (TRAF) family in T cell immunity

217 rs of tumour necrosis factor (TNF) receptor (TNFR)-mediated signalling.

218 r necrosis factor alpha (TNFalpha) receptor (TNFR) families] help drive and control intestinal inflam

219 osis factor receptor/interleukin-1 receptor, TNFR/IL-1R in mammals) is indispensable for intestinal i

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

221 antithetic effects of the two TNF receptors (TNFR) in the central nervous system, whereby TNFR1 has b

222 the precise role of the TNF-alpha receptors (TNFRs) has not been well defined using in vivo models.

223 TNF signals via two distinct receptors (TNFRs).

224 directly to tumor necrosis factor receptors (TNFRs) and disturbed the TNFalpha-TNFR interaction.

225 e family of tumor necrosis factor receptors (TNFRs) and their ligands form a regulatory signaling net

226 in-13 and 3 tumor necrosis factor receptors (TNFRs): Fas, FasL, and TNFR superfamily member 1B.

227 factor-alpha (TNF-alpha) and its receptors (TNFRs).

228 factor-alpha (TNF-alpha) and TNF receptors (TNFRs) from the cell surface.

229 stem is to encode homologs of TNF receptors (TNFRs) that block TNF-alpha function.

230 ocytosed CD137-containing vesicles recruited TNFR-associated factor (TRAF) 2 and were decorated with

231 Although the TNFR family recruits TNFR-associated factor (TRAF) molecules leading to IKKal

232 STING recruits TNFR-associated NF-kappaB kinase-binding kinase 1 which

233 FRs in hepatic stellate cells, which reduces TNFR signaling and liver fibrosis in response to injury.

234 signaling among the therapeutically relevant TNFR superfamily of receptors.

235 of three PGRN fragments, exhibited selective TNFR binding.

236 with neutralizing anti-TNF-alpha Ab, soluble TNFR, or an inhibitor of NF-kappaB, or by attenuating th

237 ve impaired signaling downstream of specific TNFR family members such as 4-1BB.

238 biquitin:NIK E3 ligase comprised of subunits TNFR-associated factors (TRAF)3, TRAF2, and cellular inh

239 whether plasma KIM-1, YKL-40, MCP-1, suPAR, TNFR-1, and TNFR-2 are associated with GFR decline in ch

240 We conclude that TNFR signaling is essential for CaOx crystal adhesion to

241 Here, we tested the hypothesis that TNFRs also have a direct role in tubular crystal deposit

242 The TNFR family member 4-1BB plays a key role in the surviva

243 The TNFR family member OX40 (CD134) is critical for optimal

244 The TNFR superfamily member 4-1BB is important in the establ

245 The TNFR-associated factor (TRAF) proteins have a vital role

246 The TNFR-Fas-caspase-8-dependent pathway provides a mechanis

247 formation of a DISC involving TNF-alpha, the TNFR-associated death domain adaptor molecule (TRADD), t

248 Although the TNFR family recruits TNFR-associated factor (TRAF) molec

249 Both the GDNF and the TNFR are large molecules that do not cross the blood-bra

250 The GDNF and the TNFR decoy receptor were re-engineered for BBB transport

251 gulation of signaling by members of both the TNFR superfamily and innate immune receptors.

252 ation of NF-kappaB signaling pathways by the TNFR: TNFR1 activated both the p65 and p52 pathways, whe

253 mune cells from knock-in mice expressing the TNFR-associated factor 6 (TRAF6) binding-defective mutan

254 Having previously described a role for the TNFR superfamily member CD27, we since screened for othe

255 OX40 is a costimulatory molecule from the TNFR family.

256 eceptor 3 (DcR3) is a soluble protein in the TNFR superfamily.

257 important adaptor molecule that mediates the TNFR family and interleukin-1 (IL-1)/Toll-like receptor

258 ducibly express a number of receptors of the TNFR and TLR families, whose signals are transduced by T

259 Combined agonist stimulation of the TNFR costimulatory receptors 4-1BB (CD137) and OX40(CD13

260 We found that 4-1BB (CD137), a member of the TNFR family, together with CD103, marked mesenteric lymp

261 Death receptors (DRs) of the TNFR superfamily contribute to antiviral immunity by pro

262 OX40 is a member of the TNFR superfamily that has potent costimulatory propertie

263 amily related gene (GITR) is a member of the TNFR superfamily that is expressed on cells of the immun

264 CD27, a member of the TNFR superfamily, is constitutively expressed in most T

265 that death receptor 3 (DR3), a member of the TNFR superfamily, is ex vivo expressed and predominantly

266 Decoy receptor 3 (DcR3), a member of the TNFR superfamily, is overexpressed in tumor cells and is

267 ced TNFR (Gitr) and Ox40, two members of the TNFR superfamily, play important roles in regulating act

268 erate agonistic Abs targeting members of the TNFR superfamily, such as OX40, 4-1BB, and GITR, express

269 gulatory functions, including members of the TNFR superfamily, the Toll-like receptor (TLR) family, t

270 se gene Pla2g7 and Tnfrsf21, a member of the TNFR superfamily.

271 signaling from OX40 (CD134), a member of the TNFR superfamily.

272 A20--an inducible feedback inhibitor of the TNFR, RIG-I, and TLR signaling pathways that broadly con

273 IgG fusion proteins, wherein the GDNF or the TNFR are fused to the heavy chain of a chimeric monoclon

274 ntitumor effects of antibodies targeting the TNFR glucocorticoid-induced TNFR-related protein (GITR;

275 We recently demonstrated that the TNFR family costimulatory molecule OX40 (CD134) is criti

276 of TNF production to models of the TLR-, the TNFR-, and the NFkappaB signaling modules, we were able

277 mbining anti-PD-L1 with agonistic Abs to the TNFR superfamily members, OX40 and CD27.

278 l costimulatory molecule that belongs to the TNFR superfamily.

279 eview will focus on agonists that target the TNFRs OX40, 4-1BB, and CD40.

280 This highlights a quantitative role of this TNFR family second signal to supplement signal 1.

281 rther underlining the key importance of this TNFR superfamily member in regulation of thymic microenv

282 lencing AC7, changes in mRNA levels of TLR1, TNFR-associated factor 6, and ST2 were seen and unchange

283 D alone and together increase levels of TNF/TNFR family members and NF-kappaB-regulated genes.

284 cognate receptor Fn14 are members of the TNF/TNFR superfamily and are upregulated in tumors.

285 receptors (TNFRs) and disturbed the TNFalpha-TNFR interaction.

286 In TNF-treated cells, TNFR1, TNFR-associated death domain protein (TRADD), Fas-associ

287 necrosis factor receptor (TNFR) 1 and TNFR2 (TNFR double knockouts); some mice were given a GATA3-spe

288 ns for the design of agonistic antibodies to TNFR as therapeutics.

289 viously reported that PGRN directly binds to TNFR and significantly enhances Treg population and stim

290 survival factor for DC, the role of the two TNFR, TNFR1 and TNFR2, in mediating these effects is poo

291 Thus, the stalk regions of the two TNFRs not only have implications for additional TNFR fam

292 dylic acid-induced formation of the upstream TNFR-associated factor (TRAF) 3/TANK-binding kinase (TBK

293 CD40 and LMP1 both use TNFR-associated factor (TRAF) adaptor proteins, but in d

294 sis factor receptor (TNFR) homologs or viral TNFR (vTNFR).

295 In vivo TNFR shedding after BDL also depended on iRhom2.

296 Whereas TNFR-induced RIPK3-dependent necroptosis requires RIPK1,

297 study was undertaken to investigate whether TNFR PLAD limits inflammatory skin injury in a mouse mod

298 ed with CD3/CD28 beads and costimulated with TNFR-selective variants.

299 Although it is normally linked with TNFR signaling pathways, TRAF5 constitutively associated

300 nent that associates with TRAF3 but not with TNFR-associated factor 2 (TRAF2).