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1 TRAF1 (TNFR-associated factor 1), TRAF2, and the inhibit
2 TRAF1 and TRAF2 form an oligomeric complex that associat
3 TRAF1 and TRAF2 preferentially form the TRAF1: (TRAF2)(2
4 TRAF1 cleavage was markedly reduced in cells that contai
5 TRAF1 expression negatively correlates with programmed d
6 TRAF1 is a member of the TRAF family, which plays import
7 TRAF1 is a member of the TRAF protein family, which regu
8 TRAF1 protein levels were also elevated in circulating B
9 TRAF1 was also highly inducible by CD40 ligand in cultur
10 TRAF1(-/-) dendritic cells show attenuated responses to
11 TRAF1(-/-) mice are viable and have normal lymphocyte de
12 TRAF1(-/-) T cells exhibit stronger than wild-type (WT)
13 TRAF1, a prosurvival signaling adaptor required for 4-1B
14 TRAF1, TRAF2, and TRAF3 appear to associate independentl
15 TRAF1, TRAF2, and TRAF3 bind to a single site in the LMP
16 TRAF1, TRAF2, and TRAF3 interacted with the same region.
17 TRAF1, TRAF2, TRAF3, and TRAF6, but not TRAF4 or TRAF5,
18 TRAF1/2 and cIAP1/2 are members of the TNF receptor-asso
19 TRAF1/C5 rs3761847 GG homozygote status was associated w
20 TRAF1/C5 rs3761847 was identified using real-time polyme
21 ecrosis factor receptor associated factor 1 (TRAF1) and defender-against cell death (DAD-1) is regula
23 ecrosis factor receptor-associated factor 1 (TRAF1) has been implicated in the regulation of antiapop
24 s factor (TNF) receptor-associated factor 1 (TRAF1) is a member of the recently defined TRAF family.
26 signaling adaptor TNFR-associated factor 1 (TRAF1) is specifically lost from virus-specific CD8 T ce
29 Bfl-1/A1, TNF receptor-associated factor-1 (TRAF1), and Fas-associated death domain protein-like int
31 crosis factor receptor-associated protein 1 (TRAF1), interleukin-1alpha (IL-1alpha), MCP-2, N-cadheri
36 iapoptosis (IAP1, Bcl-2, Bcl-X(L), Bfl-1/A1, TRAF1 and cFLIP), and invasion (MMP-9) were also downreg
37 , IAP1, IAP2, XIAP, Bcl-2, Bcl-xL, Bfl-1/A1, TRAF1 and FLIP, were all downregulated by zerumbone.
38 survivin, IAP 1, IAP 2, Bcl-x(L), Bfl-1/A1, TRAF1, and FLIP in wild-type mouse embryonic fibroblasts
39 survivin, IAP1, IAP2, XIAP, Bcl-2, Bfl-1/A1, TRAF1, and FLIP were all down-regulated by SCH 66336, wh
40 IAP2, Bcl-xL, Bcl-2, cFLIP, XIAP, Bfl-1/A1, TRAF1, and Survivin), proliferation (cyclin D1, COX2, an
46 n blot analysis confirmed that IL-1alpha and TRAF1 mRNA levels resulted in increased protein expressi
47 apoptosis (IAP1, Bfl-1/A1, Bcl-2, cFLIP, and TRAF1), proliferation (cyclin D1 and c-Myc), and angioge
48 ic upregulation of IL-1alpha (21.5-fold) and TRAF1 (27.5-fold) gene expression in tissues of Johne's
49 n of the antiapoptotic genes A1, c-IAP2, and TRAF1; inhibition of caspase 3; and protection from apop
50 optosis (IAP1 and IAP2, Bcl-2, Bcl-x(L), and TRAF1), proliferation (cyclin D1 and c-Myc), invasion (C
51 ates the antiapoptotic activity of p80HT and TRAF1 deficiency reestablishes B cell homeostasis in p80
52 was to delineate the signaling pathways and TRAF1 promoter elements responsible for phorbol ester-me
54 he evidence for association of the STAT4 and TRAF1/C5 loci with RA using imputed data from the Wellco
55 Bcl-2, Bcl-xL, IAP1,(2) MCl-1, survivin, and TRAF1), apoptosis (Bax, Bid), inflammation (COX-2), prol
56 cIAP-1/2, Bcl-2, Bcl-xL, XIAP, Survivin, and TRAF1), proliferation (cyclin D1, c-Myc, COX-2), invasio
60 ntiapoptosis (IAP1, IAP2, Bcl-2, Bcl-xL, and TRAF1), proliferation (cyclin D1 and c-Myc), and invasio
61 31)-mediated NF-kappaB activation as well as TRAF1 coactivation, and 30% of TRAF2 is associated with
65 n by LMP1(1-231) is likely to be mediated by TRAF1/TRAF2 heteroaggregates since TRAF1 is unique among
66 o to the upregulation of genes such as CD40, TRAF1, and IRF5, which encode proteins that promote B ce
68 siRNA we show that in activated CD8 T cells TRAF1 is also involved in this process and that constitu
69 hway downstream of 4-1BB in primary T cells, TRAF1 also restricts the constitutive activation of NIK
70 c-Myc), cell survival (Bcl-2, Bcl-xL, cFLIP, TRAF1, IAP1, IAP2, and survivin), invasion (matrix metal
72 In contrast, there was a high and consistent TRAF1 overexpression in EBV-induced lymphoproliferations
75 tified proapoptotic fragments Cys-RIPK1, Cys-TRAF1, Asp-BRCA1, Leu-LIMK1, Tyr-NEDD9, Arg-BID, Asp-BCL
76 ffect of reduced pulmonary TRAF1 expression, TRAF1-null (-/-) and control, BALB/c (wild-type), mice w
77 in associating with TNFR-associated factors TRAF1 and TRAF2, and the second site is similar to TNFRI
78 is factor receptor (TNFR)-associated factors TRAF1, TRAF2, TRAF3, and TRAF5 and the TNFR-associated d
79 n NF-kappaB-regulated antiapoptotic factors, TRAF1, TRAF2, c-IAP1, and c-IAP2, is most pronounced in
83 the strongest predictors of death in RA (for TRAF1/C5 GG versus AA, hazard ratio 3.85 [95% confidence
85 naling and identify a physiological role for TRAF1 as a regulator of the subcellular localization of
95 resent study, we demonstrated that the human TRAF1 mRNA has an unusually long 5'-UTR that contains in
97 s of TNF-induced TRAF1 expression identified TRAF1.NIK as a central complex linking canonical and non
98 ome-wide association studies have identified TRAF1/C5 as a rheumatoid arthritis (RA) susceptibility l
103 Thus, expression of this LMP1 domain in TRAF1-positive lymphoma cells promotes significant JNK a
106 The risk of death in RA is increased in TRAF1/C5 rs3761847 GG homozygotes and appears to be inde
107 liferation and excess cytokine production in TRAF1-deficient CD8 T cells compared with WT CD8 T cells
109 e 13-acetate (PMA) and bryostatin I, induced TRAF1 mRNA expression; pretreatment with actinomycin D b
110 tational-experimental studies of TNF-induced TRAF1 expression identified TRAF1.NIK as a central compl
111 two genes relevant to chronic inflammation: TRAF1 (encoding tumor necrosis factor receptor-associate
115 the endoplasmic reticulum stress-induced JNK/TRAF1 axis as well as the APAF-1/caspase-9 axis, activat
116 2, X chromosome-linked IAP, Bcl-2, Bcl-x(L), TRAF1, FLIP, and survivin), proliferative (cyclin D1, cy
121 ment with actinomycin D blocked PMA-mediated TRAF1 expression suggesting induction at the transcripti
122 rm-selective inhibitors blocked PMA-mediated TRAF1 mRNA and promoter stimulation; rottlerin, a select
124 inus of the molecule (TRAF2DN), which mimics TRAF1, developed lymphadenopathy and splenomegaly due to
125 ptides with progressive deletions, a minimal TRAF1, TRAF2, and TRAF3 binding region was mapped to the
126 2/p100 processing, we mathematically modeled TRAF1.NIK as a coupling signaling complex and validated
135 Transient overexpression of TRAF2, but not TRAF1, induced NF-kappaB activation and HIV-1-long termi
138 ruitment and DC activation in the airways of TRAF1(-/-) mice, suggesting that the expression of TRAF1
139 n vivo, CD11c(+)CD11b(+) DCs from airways of TRAF1(-/-) recipients were not activated, and purified d
142 ntrast to TRAF2 and TRAF3, direct binding of TRAF1, TRAF4, TRAF5, or TRAF6 to CD40 was not detected.
143 UV irradiation did not result in cleavage of TRAF1, and overexpression of the C-terminal TRAF1 fragme
144 carcinogenesis study showed that deletion of TRAF1 in mice results in a significant inhibition of ski
145 ive mutants consisting of the TRAF domain of TRAF1 and TRAF2 inhibited CD30 induction of NF-kappaB ac
147 l analyses demonstrated that TRAF domains of TRAF1, TRAF2, TRAF3, and TRAF6 formed homo-trimers in so
148 -/-) mice, suggesting that the expression of TRAF1 in resident lung cells is required for the develop
151 , we also observed an increased frequency of TRAF1(+) HIV-specific CD8 T cells 10 wk after completion
156 r results demonstrate selective induction of TRAF1 in human colon cancer cells through a Ca(2+)-depen
158 h 1 expression and HIV load and knockdown of TRAF1 in CD8 T cells from viral controllers results in d
160 ignaling and suggest that cellular levels of TRAF1 may play an important role in modulating the degra
161 cells from p80HT mice express high levels of TRAF1, an antiapoptotic protein also implicated in lymph
166 hat in EBV-transformed B lymphocytes most of TRAF1 or TRAF3 and 5% of TRAF2 are associated with LMP1
168 region appears to inhibit the recruitment of TRAF1 and TRAF2 to membrane rafts by the CTAR1 region.
170 tion of TRAF2 or combined down-regulation of TRAF1 and TRAF2 did not affect c-IAP2.MALT1-stimulated s
171 In this study, we investigated the role of TRAF1 in an adoptive transfer model of allergic lung inf
177 ulation of the IRES-dependent translation of TRAF1 may be involved in effecting the cancer cell respo
178 h Ras inhibitors had minimal to no effect on TRAF1 induction suggesting dependence on Raf, but not Ra
179 pathway activation is dependent not only on TRAF1 induction but also NIK stabilization by forming TR
181 an chronic lymphocytic leukemias overexpress TRAF1 and Bcl-2, our findings suggest that cooperation b
183 r kinase RIP (receptor-interacting protein), TRAF1, and cIAP-1 (cellular inhibitor of apoptosis prote
184 actor (TRAF) family of six adaptor proteins (TRAF1-6) links the TNFR superfamily to the nuclear facto
185 RT-1, RIP), TRAF domain containing proteins (TRAF1-6) as well as new members and adaptor proteins suc
186 previously identified TRAF family proteins (TRAF1, TRAF2, TRAF3, TRAF4, TRAF5, and TRAF6), whereas t
187 associated factor (TRAF) family of proteins, TRAF1 and TRAF2, independently bind to the intracellular
189 To determine the effect of reduced pulmonary TRAF1 expression, TRAF1-null (-/-) and control, BALB/c (
190 -kappaB pathway downstream of 4-1BB requires TRAF1, whereas cIAP1 plays a redundant role with cIAP2.
191 on in genes associated with immune response (TRAF1, RIPK3, BAT2, and TLR6), mitogen-activated protein
192 revious results showed that IL-7 can restore TRAF1 expression in virus-specific CD8 T cells in mice,
195 diated by TRAF1/TRAF2 heteroaggregates since TRAF1 is unique among the TRAFs in coactivating NF-kappa
196 ssociated factor (TRAF) family, specifically TRAF1, TRAF5, and TRAF6, but not with TRAF2, TRAF3, or T
197 PD98059 and UO126, suppressed PMA-stimulated TRAF1 promoter activity indicating a role for ERK in TRA
198 Raf-C4) significantly reduced PMA-stimulated TRAF1 promoter activity whereas transfection of dominant
199 in which TRAF1 is active in vivo, we studied TRAF1 transcripts in normal lymphoid tissue, in Epstein-
200 his finding is replicated in future studies, TRAF1/C5 genotyping could identify patients at increased
204 TRAF1, and overexpression of the C-terminal TRAF1 fragment did not enhance cell death in these cases
207 Collectively these results demonstrate that TRAF1 plays a critical role in regulating T cell activat
208 Taken together, our findings indicate that TRAF1 and TRAF2 cooperate in CD40 but not LMP1 signaling
220 Immunohistochemical analysis showed that TRAF1 expression is up-regulated in human actinic kerato
224 apping TRAF binding regions and suggest that TRAF1, TRAF2, and TRAF3 could bind competitively to one
225 We confirm association of the STAT4 and the TRAF1/C5 loci with RA bringing to 5 the number of confir
230 TRAF1 and TRAF2 preferentially form the TRAF1: (TRAF2)(2) heterotrimer, which interacts with cIA
232 (particularly the most proximal site) in the TRAF1 promoter significantly decreased PMA-mediated prom
233 6736 in the C12orf30 locus, rs3761847 in the TRAF1/C5 locus, rs2104286 in the IL2RA locus, rs7574865
234 isingly, TRAF1 and one chain of TRAF2 in the TRAF1: (TRAF2)(2): cIAP2 ternary complex mediate interac
235 tor-associated factors (TRAF), including the TRAF1/TRAF2 positive regulators and TRAF3 negative regul
236 Consistent with the desensitization of the TRAF1-binding co-stimulatory receptor 4-1BB, 4-1BBL-defi
239 ing peptide-based mutational analyses of the TRAF1/TRAF2/TRAF3 and TRAF6 binding sequences in CD40 to
241 e for association of variants mapping to the TRAF1/C5 gene was detected in the 1860 RA cases and 2930
242 ruited to the LMP1 signaling complex via the TRAF1/2/3/5 binding site within the cytoplasmic domain o
244 L), ice, TNF-alpha, TNF-beta, TNFR1, TNFR2, TRAF1, TRAF2, TRAF3, cIAP2, and tradd at the level of mR
246 interaction and established that binding to TRAF1 and TRAF2 is not required for c-IAP2.MALT1-stimula
249 inding domain that recruits A20 to the TRAF2-TRAF1 complex and a C-terminal domain that mediates inhi
250 e TNF receptor associated factors 2/1 (TRAF2/TRAF1) heterocomplex, which mediates the recruitment of
251 nally, we demonstrate that T cell-transfused TRAF1(-/-) recipient mice demonstrated impaired up-regul
252 lung injury, intratracheal TNF-alpha-treated TRAF1-/- mice exhibited marked liver injury with an appr
253 alveolar lavage from intratracheally treated TRAF1-/- mice produced more TNF-alpha than cells from tr
254 cell line transduces signals that upregulate TRAF1 levels but does not alter JAK3 levels or activatio
255 which contained the sequence PEQET, whereas TRAF1 and TRAF2 were capable of binding to either the PE
257 e resolve this paradox by showing that while TRAF1 is required for maximal activation of the classica
265 proach those of TRAF2 upon coexpression with TRAF1 and/or TRAF2, indicating that TRAF2A stability is
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