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1 IKK alpha was not required for RANKL-mediated I kappa B
2 IKK-alpha and IKK-beta formed heterodimers that interact
3 IKK-alpha and IKK-beta isozymes are found in large compl
4 IKK-alpha interacts with CREB-binding protein and in con
5 IKK-alpha was independently discovered as a NF-kappaB-in
6 IKK-alpha, however, does not relocate to the LD but tran
8 lts in production of cytokines that activate IKK-alpha and STAT3 in CaP cells to enhance hormone-free
9 polypeptide 3, X-linked (DDX3X) to activate IKK-alpha, which translocates to the nucleus and induces
10 ow that MEKK2 and MEKK3 can in vivo activate IKK-alpha and IKK-beta, induce site-specific IkappaBalph
11 hat DDX3X binds to the HCV 3'UTR, activating IKK-alpha and cellular lipogenesis to facilitate viral a
12 Here, by using a monoclonal antibody against IKK-alpha, we purify the IKK complex to homogeneity from
13 igated the effect of inhibiting the PI3K/AKT/IKK alpha pathway in regulating the inappropriate consti
14 rm of the inhibitor of kappa B kinase alpha (IKK alpha) have mammary gland defects similar to those o
15 pha-induced inhibitory kappa B kinase alpha (IKK-alpha) activation, which, in turn, resulted in a ste
16 entified two proteins, IkappaB kinase alpha (IKK-alpha) and IkappaB kinase beta (IKK-beta), that are
20 uclear factor-kappaB (IkappaB) kinase-alpha (IKK-alpha), a protein kinase that is needed for the self
23 appa B alpha phosphorylation/degradation and IKK alpha/beta and RelA phosphorylation in primary IEC d
25 ed that IKK gamma/NEMO competed with p65 and IKK alpha for binding to the N terminus of CBP, inhibiti
26 ction, the HCV 3'UTR redistributes DDX3X and IKK-alpha to speckle-like cytoplasmic structures shown t
27 tion, the HCV 3'UTR interacts with DDX3X and IKK-alpha, which redistribute to speckle-like cytoplasmi
28 tors of IKK-alpha suppress HCV infection and IKK-alpha-induced lipogenesis, offering a proof-of-conce
29 protein 1 (LRP1), and the NF-kappaB p65 and IKK-alpha/beta signaling pathways in modulating neuroinf
30 e therefore examined whether RANKL, RANK and IKK-alpha are also involved in mammary/breast cancer met
32 composed of IkappaB kinase beta (IKK-beta), IKK-alpha, and IKK-gamma/N, leading to changes in NF-kap
33 her kinase dead (KD) IKK alpha, which blocks IKK alpha kinase activity, KD AKT, which blocks AKT acti
37 s composed of a heterodimer of the catalytic IKK alpha and IKK beta subunits and a presumed regulator
40 ctivating inhibitor of kappaB kinase complex IKK-alpha/beta and active transcription factor NF-kappaB
42 ddition to failed epidermal differentiation, IKK-alpha-deficient mice exhibit abnormal skeletal and c
44 g mouse embryonic fibroblasts lacking either IKK alpha or IKK beta, we found that IKK beta played an
45 dition, dominant negative versions of either IKK-alpha or IKK-beta abolish NF-kappaB activation induc
46 ving dynamic associations with HCV elements, IKK-alpha, SGs, and LDs for its critical role in HCV inf
51 e nuclear factor kappaB/IkappaB cascade (ie, IKK-alpha,-beta,-gamma/NEMO and CARMA/MALT1/Bcl10 comple
52 lls lacking either catalytic subunit of IKK (IKK-alpha or IKK-beta) fail to induce autophagy in respo
53 uced activation of the IkappaB kinases (IKK) IKK-alpha and IKK-beta is a key step involved in the act
54 gene expression was significantly blunted in IKK alpha(-/-) cells, including osteoclast-specific gene
57 postulated that the morphogenetic defects in IKK-alpha-deficient mice are not caused by reduced NF-ka
58 eless, mouse embryo fibroblasts deficient in IKK-alpha are defective in the induction of NF-kappaB-de
60 e activity of IL-1beta and TNF-alpha induced IKK-alpha/beta towards NF-kappaB p65, resulting in a red
65 siently transfecting either kinase dead (KD) IKK alpha, which blocks IKK alpha kinase activity, KD AK
66 omplex, which is composed of the two kinases IKK alpha and IKK beta and the regulatory subunit IKK ga
67 D40 engagement activated the IkappaB kinases IKK-alpha and IKK-beta and stimulated IkappaBalpha phosp
75 construct with either the dominant negative IKK-alpha or the repressors of NF-kappaB, the IkappaB-al
77 ivation of NF-kappa B inducing kinase (NIK)--IKK alpha/beta complex leading to I kappa B alpha phosph
78 -1-inducible IKK complexes that contain NIK, IKK-alpha, IKK-beta, IkappaB-alpha, NF-kappaB/RelA and a
80 ates NF-kappa B via TLR2-TAK1-dependent NIK--IKK alpha/beta-I kappa B alpha and MKK3/6--p38 MAP kinas
84 alicylate, an inhibitor of IKK beta, but not IKK alpha, activity, inhibited IL-2 promoter activation
87 IKK genes have shown that IKK-beta, but not IKK-alpha, is critical for cytokine-induced IkappaB degr
90 hibit NF-kappaB activation via inhibition of IKK alpha or IKK beta, whereas proteosome inhibitors ins
95 Here we demonstrate nuclear accumulation of IKK-alpha after cytokine exposure, suggesting a nuclear
96 d region (UTR), leading to the activation of IKK-alpha and a cascade of lipogenic signaling to facili
98 inflammatory infiltration and activation of IKK-alpha, which stimulates metastasis by an NF-kappaB-i
99 d that IKK is composed of similar amounts of IKK-alpha, IKK-beta and two other polypeptides, for whic
101 ugh the basal level of protein expression of IKK-alpha or IKK-beta are the same in both Hs294T and RP
106 gene expression is suppressed by the loss of IKK-alpha and this correlates with a complete loss of ge
112 These results define a new nuclear role of IKK-alpha in modifying histone function that is critical
113 osteoclast differentiation was dependent on IKK alpha, suggesting that synergy between RANKL and TNF
114 ull mice, which completely lack osteoclasts, IKK alpha(-/-) mice did possess normal numbers of TRAP(+
116 show that NIK preferentially phosphorylates IKK-alpha over IKK-beta, leading to the activation of IK
117 amic associations with HCV RNA and proteins, IKK-alpha, SG, and LD surfaces for its crucial role in t
119 PKK-mediated NF-kappa B activation required IKK alpha and IKK beta but not IKK gamma, the regulatory
120 g of IKKgamma to the IKK catalytic subunits, IKK-alpha and -beta, and attenuates the IKK catalytic ac
122 anced activation of the protein kinases TAK, IKK-alpha/beta, c-Jun N-terminal kinases, and p38alpha m
124 nd regulation of NF-kappaB activity and that IKK-alpha can only partially compensate for the loss of
127 mmunoprecipitation (ChIP) assays reveal that IKK-alpha was recruited to the promoter regions of NF-ka
133 gnals in NK cells involves activation of the IKK alpha kinase, inhibitory protein kappa B alpha degra
135 expression was accompanied by dampening the IKK-alpha/beta-NF-kappaB p65 pathway, resulting in decre
137 KK epsilon, two kinases distantly related to IKK alpha/beta, but the underlying mechanisms remained u
140 teoclastogenesis was observed in vitro using IKK alpha(-/-) hematopoietic cells treated with colony-s
142 osphorylated IkappaB constitutively, whereas IKK-alpha was not active in the absence of cell stimulat
143 cytokine-induced NF-kappaB function, whereas IKK-alpha is thought to be involved in other regulatory
144 observations raised the question of whether IKK-alpha might regulate a previously undescribed step t
146 ced p65 phosphorylation on serine 536, while IKK alpha was partially required for the p65 phosphoryla
147 keletal defects that are not associated with IKK alpha-kinase activity, we wished to directly examine
148 294T and RPE cells, immunoprecipitation with IKK-alpha antibody combined with activity assay reveal a
149 the truncated NEMO protein interactions with IKK-alpha, IKK-beta, TNF receptor-associated factor 6, T