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1 associated with the upstream activator NIK (NF-kappaB-inducing kinase).
2 c mutation in the MAP3K14 gene encoding NIK (NF-kappaB-inducing kinase).
3 nd induce proteasome-mediated degradation of NF-kappaB inducing kinase.
4 ty against IkappaBalpha or its activation by NF-kappaB-inducing kinase.
5 sociated kinase, TNFR-associated factor, and NF-kappaB-inducing kinase.
6 -kappaB activation but were not dependent on NF-kappaB-inducing kinase.
7 ogene homolog B (RELB) activated by means of NF-kappaB-inducing kinase.
8 nd prevents Monarch-1-induced proteolysis of NF-kappaB-inducing kinase.
9 inducing proteasome-mediated degradation of NF-kappaB-inducing kinase.
11 nant negative (DN) inhibitors DN-TRAF2 or DN-NF-kappaB-inducing kinase also abolished VP8*-, VP4-, or
12 duced NF-kappaB reporter activity induced by NF-kappaB inducing kinase and IkappaB alpha kinase but n
14 esults suggest roles for the IkappaB kinases NF-kappaB-inducing kinase and mitogen-activated protein
15 cting protein (RIP), which in turn activates NF-kappaB-inducing kinase and phosphorylates IkappaB.
16 B kinase-alpha and several fold increases in NF-kappaB-inducing kinase and RelB, which were predomina
18 ated kinase 1, receptor-interacting protein, NF-kappaB-inducing kinase, and IkappaB kinase beta was a
19 th domain protein, TNFR-associated factor-2, NF-kappaB-inducing kinase, and IkappaBalpha kinase but n
20 th domain, TNF receptor-associated factor-2, NF-kappaB-inducing kinase, and IkappaBalpha kinase, were
22 th domain protein, TNFR-associated factor 2, NF-kappaB-inducing kinase, and IKK, but not that activat
23 ceptor-associated death domain, TRAF2, TAK1, NF-kappaB-inducing kinase, and IKKbeta was inhibited by
24 strate that receptor-interacting protein and NF-kappaB-inducing kinase are dispensable for vFLIP K13-
25 ion, including TRAF2, TRAF6, RIP, IRAK2, and NF-kappaB-inducing kinase as well as the IkappaB kinases
27 sion of TNFR1, TNFR-associated factor-2, and NF-kappaB-inducing kinase, but not that activated by the
28 ILF were present in the small intestine from NF-kappaB-inducing kinase-deficient alymphoplasia mice,
29 r-3 to the Toll-like receptor/MyD88 complex, NF-kappaB-inducing kinase-dependent IkappaB kinase-alpha
31 smooth muscle dysregulation, LIGHT promoted NF-kappaB-inducing kinase-dependent noncanonical nuclear
34 ding, and IL-8 secretion, whereas IKK1dn and NF-kappaB-inducing kinase dominant negative do not have
37 ation, such as receptor-interacting protein, NF-kappaB-inducing kinase, IkappaB kinase (IKK) 1, IKK2,
38 mor necrosis factor receptor (TNFR)1, TNFR2, NF-kappaB-inducing kinase, IkappaB kinase complex (IKK),
39 Rituximab decreased the phosphorylation of NF-kappaB-inducing kinase, IkappaB kinase, and IkappaB-a
40 paB translocation-dependent pathway involves NF-kappaB-inducing kinase-IkappaB kinase beta/gamma-depe
41 th domain, TNF receptor-associated factor-2, NF-kappaB-inducing kinase, IkappaBalpha kinase, and p65
42 eath domain, TNF receptor-associated factor, NF-kappaB-inducing kinase, IkappaBalpha kinase, and p65.
43 ssion activated by TNF, TNFR1, TRADD, TRAF2, NF-kappaB-inducing kinase, IkappaBalpha kinase, and the
44 eath domain/TNF receptor-associated factor 2/NF-kappaB-inducing kinase/IkappaBalpha kinase was interr
45 n and TRAF2 plasmids; NF-kappaB activated by NF-kappaB-inducing kinase, IKK or p65, however, was mini
46 ponse to tumor necrosis factor (TNF) and the NF-kappaB-inducing kinase-IKKalpha signaling pathway.
47 omponents (Fas receptor-interacting protein, NF-kappaB-inducing kinase, IKKbeta) of the NF-kappaB act
48 d factor-6, TGF-beta-activated kinase-1, and NF-kappaB-inducing kinase in an IL-1-dependent manner, s
50 atory importance of the survival kinase NIK (NF-kappaB-inducing kinase) in genetically engineered mur
51 sense RNA into 293 or HeLa cells blocks NIK (NF-kappaB-inducing kinase)-induced phosphorylation of th
52 In summary, we conclude that plumbagin is a NF-kappaB-inducing kinase inhibitor with dual anabolic a
55 d induce proteasomal-mediated degradation of NF-kappaB Inducing Kinase (NIK) and repress non-canonica
58 ing relB activation further, we found stable NF-kappaB inducing kinase (NIK) protein in several HL ce
62 am signaling targets, nuclear factor-kappaB (NF-kappaB)-inducing kinase (NIK) and p65 nuclear factor
63 a-light-chain-enhancer of activated B cells (NF-kappaB)-inducing kinase (NIK) as a potential drug tar
66 e identified hepatic nuclear factor kappa B (NF-kappaB)-inducing kinase (NIK), a Ser/Thr kinase, as a
67 endent degradation of nuclear factor-kappaB (NF-kappaB)-inducing kinase (NIK), an action required for
69 ns in endothelial cells (ECs) by stabilizing NF-kappaB-inducing kinase (NIK) and activating noncanoni
70 cytokines requires the successive action of NF-kappaB-inducing kinase (NIK) and an IKB-kinase (IKK)
71 ue pathway by extracellular stimuli requires NF-kappaB-inducing kinase (NIK) and de novo protein synt
73 Transient overexpression of kinase-deficient NF-kappaB-inducing kinase (NIK) and IkappaB kinase (IKK)
74 cytokines requires the successive action of NF-kappaB-inducing kinase (NIK) and IkappaB kinase-alpha
75 the sequential activation of the downstream NF-kappaB-inducing kinase (NIK) and IkappaB-specific kin
76 eceptor- or CD40L-activated association with NF-kappaB-inducing kinase (NIK) and interleukin-1 recept
77 hysiological processing of p100 triggered by NF-kappaB-inducing kinase (NIK) and its downstream kinas
78 controlled event is regulated positively by NF-kappaB-inducing kinase (NIK) and its downstream kinas
80 as absent in alymphoplasia mice deficient in NF-kappaB-inducing kinase (NIK) and NIK knockout mice.
81 rmore, we show that the EGFR associates with NF-kappaB-inducing kinase (NIK) and provide evidence sug
82 ciated factor-1 (TRAF-1) that directly binds NF-kappaB-inducing kinase (NIK) and stabilizes it from d
83 Mechanistically, SM-mediated activation of NF-kappaB-inducing kinase (NIK) and the transcription fa
85 on of receptor-interaction protein 1 (RIP1), NF-kappaB-inducing kinase (NIK) and themselves, and regu
86 ed in the noncanonical pathway downstream of NF-kappaB-inducing kinase (NIK) and TNF receptor family
87 cytokines involves the successive action of NF-kappaB-inducing kinase (NIK) and two IkappaB kinases,
92 CTAR1-mediated EGFR induction required the NF-kappaB-inducing kinase (NIK) but not the IkappaB kina
94 the serine/threonine-specific protein kinase NF-kappaB-inducing kinase (NIK) develop a HES-like disea
95 armacological activation of the noncanonical NF-kappaB-inducing kinase (NIK) disrupts glucose homeost
97 paB) signaling in resting cells by targeting NF-kappaB-inducing kinase (NIK) for ubiquitin-dependent
101 en-activated protein kinase kinase kinase 14/NF-kappaB-inducing kinase (NIK) in the activation of NF-
103 ble to synergistic effects on phosphorylated NF-kappaB-inducing kinase (NIK) in the non-canonical pat
104 a dominant negative mutant of IKKbeta or the NF-kappaB-inducing kinase (NIK) inhibited pIC-induced ge
105 n contrast, a kinase-deficient mutant of the NF-kappaB-inducing kinase (NIK) inhibits both CD3/CD28 a
114 -kappaB pathway, either by overexpression of NF-kappaB-inducing kinase (NIK) or by treatment with the
117 oncanonical NF-kappaB pathway as measured by NF-kappaB-inducing kinase (NIK) protein levels and proce
119 Homozygosity for the aly point mutation in NF-kappaB-inducing kinase (NIK) results in alymphoplasia
120 1/I kappa B kinase alpha (IKK1/IKKalpha) and NF-kappaB-inducing kinase (NIK) to direct processing of
123 receptor-associated factor 5 (TRAF5), TRAF6, NF-kappaB-inducing kinase (NIK), and IkappaB kinase (IKK
124 uced by TNFR1, TNFR-associated factor 2, and NF-kappaB-inducing kinase (NIK), but not that activated
125 ced the CGN-induced increases in KC, phospho-NF-kappaB-inducing kinase (NIK), cytoplasmic NF-kappaB p
126 olism or overexpression of dominant negative NF-kappaB-inducing kinase (NIK), IkappaB kinase (IKK), o
128 mphoplasia (aly/aly) mice, which lack active NF-kappaB-inducing kinase (NIK), show mild osteopetrosis
129 re, we show that IKKalpha and its activator, NF-kappaB-inducing kinase (NIK), support the expansion o
130 deficient cells results from accumulation of NF-kappaB-inducing kinase (NIK), the essential kinase me
131 ent of the noncanonical NF-kappaB pathway is NF-kappaB-inducing kinase (NIK), which functions togethe
133 appaB pathway hinges on the stability of the NF-kappaB-inducing kinase (NIK), which is kept at low le
135 showed that RA ST contains ECs that express NF-kappaB-inducing kinase (NIK), which is pivotal in LTb
136 alternative or second pathway proceeded via NF-kappaB-inducing kinase (NIK)-, IKKalpha-, and protein
137 IKK-alpha was independently discovered as a NF-kappaB-inducing kinase (NIK)-associated protein in a
140 nsulin resistance; however, the noncanonical NF-kappaB-inducing kinase (NIK)-NF-kappaB2 pathway is no
153 ith TRADD, RIP, and TRAF2; activation of the NF-kappaB-inducing kinase (NIK); activation of the Ikapp
156 activate NF-kappaB by acting upstream of the NF-kappaB-inducing kinase, NIK, and the IkB kinase, IKKa
157 Overexpression of a kinase-dead mutant of NF-kappaB-inducing kinase or IkappaB kinase-beta but not
158 of dominant negative mutants of either NIK (NF-kappaB-inducing kinase) or IKKbeta (IkappaB kinase be
159 g protein, TNF receptor-associated factor 2, NF-kappaB-inducing kinase, or MyD88, we hypothesized tha
160 been suggested through indirect studies that NF-kappaB-inducing kinase, or NIK, may be involved in No
161 rowth factor beta-activated kinase-1 (TAK1), NF-kappaB-inducing kinase, or phosphatidylinositol 3-kin
162 shown that NF-kappaB is activated through a NF-kappaB-inducing kinase/p21-activated kinase 1 pathway
163 inally, the Src/Rac1/MKK3/6/p38 and Src/TAK1/NF-kappaB-inducing kinase pathways exhibited cross-talk
165 blocked TNF receptor-associated factor-2 and NF-kappaB-inducing kinase reporter gene expression, hCG
166 rimarily activates NF-kappaB through a TRAF2-NF-kappaB-inducing kinase signaling pathway and that VP4
167 at the TNF receptor-associated factor 2 and NF-kappaB-inducing kinase sites by oleandrin, thus suppr
168 kappaB pathway on colonic fibroblasts with a NF-kappaB-inducing kinase small molecule inhibitor impai
169 und that plumbagin inhibited the activity of NF-kappaB inducing kinase, the key molecule that control
170 kinases of the NF-kappaB activation pathway, NF-kappaB-inducing kinase, transforming growth factor be
171 TNFR1, TNF receptor-associated factor 2, and NF-kappaB-inducing kinase was also abrogated by IFN-alph
174 a, such as IkappaB kinase alpha and beta and NF-kappaB-inducing kinase, were also shown to interact w
175 IRAK, TNF receptor-associated factor 6, and NF-kappaB-inducing kinase, when coexpressed with TLR2, a
176 Similarly, a kinase-deficient mutant of NIK (NF-kappaB-inducing kinase), which represents an upstream
177 Moreover, deletion of the gene encoding NF-kappaB-inducing kinase, which is known to modulate IK