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1                                              IKK beta overexpression in a Jurkat cell line resulted i
2                                              IKK beta/NF-kappaB signaling decreases chronic Helicobac
3                                              IKK-beta and IKK-gamma are critical for cytokine-induced
4                                              IKK-beta deficiency results in defective induction of HI
5                                              IKK-beta is also essential for HIF-1alpha accumulation i
6                                              IKK-beta is modestly activated in hypoxic cell cultures
7                                              IKK-beta removal from enterocytes, however, also resulte
8                                              IKK-beta was expressed primarily in the liver, kidney an
9                                              IKK-beta-deficient embryonic fibroblasts have both reduc
10 se data suggest that paclitaxel may activate IKK-beta via conventional PKC isotypes, resulting in NF-
11  constitutively overexpressing kinase-active IKK-beta, an essential kinase for NF-kappaB activation,
12 is composed of similar amounts of IKK-alpha, IKK-beta and two other polypeptides, for which we obtain
13 e IKK complexes that contain NIK, IKK-alpha, IKK-beta, IkappaB-alpha, NF-kappaB/RelA and a protein of
14 ed NEMO protein interactions with IKK-alpha, IKK-beta, TNF receptor-associated factor 6, TNF receptor
15 esults suggest that it involves an IKK alpha/IKK beta-independent mechanism.
16 r, these data demonstrate the presence of an IKK beta-mediated signaling pathway that is activated by
17           Cotransfection experiments with an IKK beta negative dominant completely inhibit CD23 induc
18 ex, which includes the IKK alpha (IKK-1) and IKK beta (IKK-2) kinases.
19 is composed of the two kinases IKK alpha and IKK beta and the regulatory subunit IKK gamma/nuclear fa
20 NF-kappa B activation required IKK alpha and IKK beta but not IKK gamma, the regulatory subunit of th
21 a heterodimer of the catalytic IKK alpha and IKK beta subunits and a presumed regulatory protein term
22 radation by I kappa B kinases (IKK alpha and IKK beta).
23 ne kinases, I kappa B kinase (IKK) alpha and IKK beta, and increased NF-kappa B DNA binding activity.
24   Expression and the ratios of IKK alpha and IKK beta, which homo- and heterodimerize, varied among c
25 turnover and the activities of IKK alpha and IKK beta.
26 -negative versions of JNK kinase, c-Jun, and IKK beta interfered In CD3- plus CD28-induced CD28RE/AP-
27  activated the IkappaB kinases IKK-alpha and IKK-beta and stimulated IkappaBalpha phosphorylation.
28               We conclude that IKK-alpha and IKK-beta can mediate the NF-kappaB-inducing activity of
29 e show herein that recombinant IKK-alpha and IKK-beta can, in fact, directly phosphorylate IkappaB al
30                                IKK-alpha and IKK-beta formed heterodimers that interacted with NIK.
31                            The IKK-alpha and IKK-beta genes are distinct but evolutionarily conserved
32  induce the activation of both IKK-alpha and IKK-beta in vivo.
33 n of the IkappaB kinases (IKK) IKK-alpha and IKK-beta is a key step involved in the activation of the
34                                IKK-alpha and IKK-beta isozymes are found in large complexes of relati
35                 We showed that IKK-alpha and IKK-beta were coexpressed in most human adult tissues as
36 kappaB kinase-alpha and -beta (IKK-alpha and IKK-beta), the catalytic subunits of the IKK complex, ph
37                These subunits, IKK-alpha and IKK-beta, are protein kinases whose function is needed f
38 and MEKK3 can in vivo activate IKK-alpha and IKK-beta, induce site-specific IkappaBalpha phosphorylat
39 IKK is made up of two kinases, IKK-alpha and IKK-beta, which phosphorylate I(kappa)B, leading to its
40 oprotein-specific signaling to IKK-alpha and IKK-beta.
41 ing these two IkappaB kinases, IKK-alpha and IKK-beta.
42 (NIK) and two IkappaB kinases, IKK-alpha and IKK-beta.
43 proteins previously shown to inhibit JNK and IKK-beta activation, respectively.
44 cantly decreased the expression of NF-kB and IKK-beta in THP-1 cells.
45 ed protein in a yeast two-hybrid screen, and IKK-beta was also identified by homology screening.
46  by TNFR1, TRADD, TRAF2, NIK, TAK1/TAB1, and IKK-beta.
47 nding protein 1 (TAB1):I kappaB kinase beta (IKK beta) complexes, which led to the stimulation of a T
48 ectopic expression of I-kappa B kinase-beta (IKK beta) enhanced reporter gene activity.
49 ctive cross-talk with I kappa B kinase-beta (IKK beta).
50 ing pathway involving I kappaB kinases beta (IKK beta), tuberous sclerosis complex 1 (TSC1), and mamm
51 ase C- (PKC-), inhibitor kappaB kinase beta (IKK-beta), c-Jun N-terminal kinase (JNK), or phospho-JNK
52 ase complex composed of IkappaB kinase beta (IKK-beta), IKK-alpha, and IKK-gamma/N, leading to change
53 e alpha (IKK-alpha) and IkappaB kinase beta (IKK-beta), that are present in a tumor necrosis factor a
54                         IkappaB kinase beta (IKK-beta, encoded by Ikbkb) is a central coordinator of
55                         IkappaB kinase-beta (IKK-beta) activated NF-kappaB when overexpressed and pho
56 quinoline inhibitors of IkappaB kinase-beta (IKK-beta) are described.
57 nhibitor of NF-kappaB (IkappaB) kinase-beta (IKK-beta), a protein kinase that phosphorylates the NF-k
58 ic immunity mediated by IkappaB kinase-beta (IKK-beta), nuclear factor kappaB (NF-kappaB) and related
59  its upstream activator IkappaB kinase-beta (IKK-beta, encoded by Ikbkb) in the mediobasal hypothalam
60 f nuclear factor kappaB kinase subunit beta (IKK-beta)-nuclear factor of kappa light polypeptide gene
61                            SCFHOS-ROC1 binds IKK beta-phosphorylated I kappa B alpha and catalyzes it
62 -terminal truncation mutant that still binds IKK-beta blocks the activation of IKK and NF-kappaB.
63  IKK-beta knockout mice showed that blocking IKK-beta activity significantly prolonged tail bleeding
64                                         Both IKK-beta and NF-kappaB p65 were required for TNF-alpha-i
65 venting ageing-related hypothalamic or brain IKK-beta and NF-kappaB activation.
66 state cancer cells, with less involvement by IKK beta.
67 ngs demonstrate the importance of liver cell IKK-beta in hepatic insulin resistance and the central r
68  genetic manipulation (platelet factor 4 Cre:IKK-beta(flox/flox)), blocked SNAP-23 phosphorylation, p
69 ominant negative IkappaB-beta or kinase dead IKK-beta significantly attenuated IL-18-induced HCME cel
70 plasmids harbouring nleH1 or nleH2 decreased IKK-beta-induced NF-kappaB activity and attenuated TNF-a
71                    Adenoviral delivery of dn IKK beta or treatment with wortmannin inhibited B. vulga
72 churis infection ablates the requirement for IKK-beta in IECs to promote CD4+ T(H)2 cell-dependent im
73 e in vivo function of IKK-beta, we generated IKK-beta-deficient mice.
74                                       Hence, IKK-beta is an important physiological contributor to th
75 terodimeric IKK alpha/beta and a homodimeric IKK beta complex.
76                                     However, IKK beta phosphorylates the N-terminal serines of I kapp
77 ve effects of the activation of hypothalamic IKK-beta and NF-kappaB, which underlie obesity-related h
78  genes such as CDKN1A (p21), CD9, and IKBKB (IKK-beta), genes known to exhibit key biological roles i
79  is mediated by the I kappa B kinase 2 (IKK2/IKK beta).
80 activity, suppressed PTEN gene expression in IKK beta(+/+) cells but not in IKK beta(-/-) cells, whic
81 expression in IKK beta(+/+) cells but not in IKK beta(-/-) cells, which are deficient in the NF-kappa
82 es of the IKK complex are greatly reduced in IKK-beta-deficient cells.
83             Conversely, only kinase-inactive IKK beta interfered in the activation of the IL-2 promot
84 ted the activation of IKK complex, including IKK-beta.
85 n and sodium salicylate specifically inhibit IKK-beta activity in vitro and in vivo.
86                               Interestingly, IKK-beta phosphorylated IkappaB constitutively, whereas
87 ivation of a serine kinase cascade involving IKK-beta.
88 terminal serines of both I kappa B isoforms, IKK beta is an efficient kinase for those residues in I
89 mulates the activity of the I kappa B kinase IKK beta, Cdc42 and Rho activate NF kappa B without acti
90 terestingly, the activity of IkappaB kinase (IKK-beta), which plays an essential role in NF-kappaB ac
91 kinase (JNK) and inhibitor of kappaB kinase (IKK-beta), stress kinases implicated in insulin resistan
92   Here we show, with the use of mice lacking IKK-beta in different cell types, that NF-kappaB is a cr
93 aling during the clamp in awake mice lacking IKK-beta.
94  controlled by IkappaB kinases (IKK), mainly IKK-beta, needed for phosphorylation-induced degradation
95       Unlike the response in wild-type mice, IKK-beta knockout mice did not exhibit altered skeletal
96                                    Moreover, IKK beta, but not IKK alpha, overexpression enhanced tra
97 e regulation and global expression of murine IKK-beta, and localize the IKK-beta gene to mouse chromo
98 mediated overexpression of dominant negative IKK-beta or IkappaB-alpha did not increase UV-induced ap
99 ression activated by TNF, TNFR1, TRAF2, NIK, IKK-beta, and the p65 subunit of NF-kappaB.
100 show that Tax binds to neither IKK-alpha nor IKK-beta but instead complexes directly with IKK-gamma,
101 onstrate that CD3/CD28-induced activation of IKK beta and expression of Bcl-xL promote the survival o
102                  Like Dbl, Rac activation of IKK beta is mediated by the serine/threonine kinases NIK
103        Consequently, transient expression of IKK beta diminished the capacity of the inhibitors to bl
104           Sodium salicylate, an inhibitor of IKK beta, but not IKK alpha, activity, inhibited IL-2 pr
105 and cyclopentenone PGs, direct inhibitors of IKK beta, interfered in the activation of the Bcl-xL pro
106 n IEC-6 cells, suggesting a critical role of IKK beta and phosphatidylinositol 3-kinase/Akt in bacter
107 tant proteins that act as superrepressors of IKK beta and I kappa B alpha inhibited the up-regulated
108                   Replacement of Cys(179) of IKK-beta with alanine abolished the effect of nimbolide,
109                                  Ablation of IKK-beta in enterocytes prevented the systemic inflammat
110 conclusion, obesity-associated activation of IKK-beta and NF-kappaB in the mediobasal hypothalamus--p
111                              The activity of IKK-beta was stimulated by tumor necrosis factor and int
112   These results indicate that the balance of IKK-beta-dependent gene expression in the intestinal epi
113        Mice with an IEC-specific deletion of IKK-beta show a reduced expression of the epithelial-cel
114              At 15.5 days, the expression of IKK-beta was further restricted to specific tissues of t
115 pression of a catalytically inactive form of IKK-beta blocked cytokine-induced NF-kappaB activation.
116         To elucidate the in vivo function of IKK-beta, we generated IKK-beta-deficient mice.
117                       S-glutathionylation of IKK-beta Cys-179 is reversed by glutaredoxin (GRX), whic
118 ensitizes cells to oxidative inactivation of IKK-beta and dampens TNF-alpha-induced IKK and NF-kappaB
119 ry, high-dose salicylate and inactivation of IKK-beta prevent fat-induced insulin resistance in skele
120                Pharmacological inhibition of IKK-beta during IgE-dependent stimulation strongly reduc
121                                Inhibition of IKK-beta, either pharmacologically (with BMS-345541, BAY
122                We suggest that inhibition of IKK-beta, especially in myeloid cells, may be used to tr
123 ated in part by their specific inhibition of IKK-beta, thereby preventing activation by NF-kappaB of
124 lization of IL-6 or salicylate inhibition of IKK-beta.
125 atment with salicylate, a known inhibitor of IKK-beta.
126 an only partially compensate for the loss of IKK-beta.
127                    To understand the role of IKK-beta in insulin resistance, we used mice lacking thi
128 fect on interacting with the binding site of IKK-beta due to the interaction of anti-inflammatory ami
129            Hit-generation chemistry based on IKK-beta active-site knowledge yielded a weakly potent b
130 onic fibroblasts lacking either IKK alpha or IKK beta, we found that IKK beta played an essential rol
131 aB activation via inhibition of IKK alpha or IKK beta, whereas proteosome inhibitors instead suppress
132 ppa B without activating either IKK alpha or IKK beta.
133 ant negative versions of either IKK-alpha or IKK-beta abolish NF-kappaB activation induced by MEKK2 o
134  level of protein expression of IKK-alpha or IKK-beta are the same in both Hs294T and RPE cells, immu
135 ither catalytic subunit of IKK (IKK-alpha or IKK-beta) fail to induce autophagy in response to cellul
136 preferentially phosphorylates IKK-alpha over IKK-beta, leading to the activation of IKK-alpha kinase
137 naling, demonstrated by reduction of phospho-IKK-beta, -IkappaB-alpha, and p65 nuclear translocation
138 , we found high expression of phosphorylated IKK beta (pIKK beta) and phosphorylated S6K1 (pS6K1) in
139 ies with IKK inhibitors or platelet-specific IKK-beta knockout mice showed that blocking IKK-beta act
140                                         TAB1:IKK beta complexes could only be detected in NMuMG cells
141 exes, which led to the stimulation of a TAK1:IKK beta:p65 pathway.
142  our findings have defined a novel TAB1:TAK1:IKK beta:NF-kappaB signaling axis that forms aberrantly
143     In summary, our results demonstrate that IKK beta plays an essential role in the LPS-induced p65
144  either IKK alpha or IKK beta, we found that IKK beta played an essential role in LPS-induced p65 pho
145                  These results indicate that IKK-beta is crucial for liver development and regulation
146    Mechanistic studies further revealed that IKK-beta and NF-kappaB inhibit gonadotropin-releasing ho
147 dies of the murine IKK genes have shown that IKK-beta, but not IKK-alpha, is critical for cytokine-in
148 cific tissues of the embryo, suggesting that IKK-beta is a developmentally regulated protein kinase.
149 B kinase (IKK) complex, predominantly by the IKK beta catalytic subunit, and requires the regulatory
150 lls with the mTOR inhibitor rapamycin or the IKK beta inhibitor Bay 11-7082 suppressed bile acid-indu
151 ation of these specific PKC isoforms and the IKK-beta/IkappaB/NFkappaB pathway remains to be establis
152 ression of murine IKK-beta, and localize the IKK-beta gene to mouse chromosome 8A3-A4.
153  unique, low molecular weight complex of the IKK-beta subunit can be observed in MP-12-infected cells
154 apped to human chromosome 10q24, whereas the IKK-beta gene locus was localized to human chromosome 8p
155 t bile acid can deregulate TSC1/mTOR through IKK beta signaling, which may play a critical role in EA
156                                        Thus, IKK-beta acts locally in liver and systemically in myelo
157 K alpha (the IKK kinase activated by Akt) to IKK beta were most sensitive to PI 3-kinase inhibitors.
158 ype cells in which the ratio of IKK alpha to IKK beta is low.
159 ibition is due to binding of these agents to IKK-beta to reduce ATP binding.
160 minant-active MEKK1 also induced transfected IKK beta, but not IKK alpha, activity.
161 mplicated in the activation of NF-kappaB via IKK-beta, the effect of paclitaxel on PKC activation was
162 pha/IKK1 subunit of the IKK complex, whereas IKK beta/IKK2, receptor-interacting protein, and NF-kapp
163 with leukocytes, including B cells, in which IKK-beta activation results in production of cytokines t
164                                        While IKK-beta was expressed ubiquitously throughout the mouse
165 ibitor reduced the association of Hsp27 with IKK beta and thus resulted in increased IKK activity.
166  p38, enhanced the association of Hsp27 with IKK beta to result in decreased IKK activity.
167      IKK-gamma interacts preferentially with IKK-beta and is required for the activation of the IKK c

 
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