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1 IkappaBbeta degradation releases NF-kappaB dimers which
2 IkappaBbeta derives its high affinity toward NF-kappaB d
3 IkappaBbeta expression in haploid spermatids is likely r
4 IkappaBbeta is a member of the IkappaB family of structu
5 IkappaBbeta mRNA knock down also reduced resistance to s
6 IkappaBbeta mRNA knock down selectively abrogated the re
7 IkappaBbeta, a major isoform of IkappaB, can sequester N
8 IkappaBbeta, one of the major IkappaB proteins, is only
9 that mitochondrial stress signaling uses an IkappaBbeta-initiated NFkappaB pathway that is distinct
10 ct with the PEST domains of IkappaBalpha and IkappaBbeta [inhibitors of the transcription factor nucl
13 gradation of the inhibitors IkappaBalpha and IkappaBbeta and the concomitant release of NF-kappaB.
15 ecificity of HTLV-1 Tax for IkappaBalpha and IkappaBbeta at the protein level, Tax selectively stimul
16 We show that although both IkappaBalpha and IkappaBbeta bind to NF-kappaB with similar global archit
19 of DENV protease to induce IkappaBalpha and IkappaBbeta cleavage and trigger hemorrhage development.
20 nase activation to regulate IkappaBalpha and IkappaBbeta degradation and synthesis, and promote Ikapp
21 Most agents that activate IkappaBalpha and IkappaBbeta degradation do not induce rapid degradation
25 n induced the expression of IkappaBalpha and IkappaBbeta in thymocytes and down-regulated NF-kappaB D
27 taneous proteolysis of both IkappaBalpha and IkappaBbeta isoforms; IkappaBgamma is inert to TNFalpha
28 se results demonstrate that IkappaBalpha and IkappaBbeta play unique injury context-specific roles in
29 ists induced an increase in IkappaBalpha and IkappaBbeta protein levels, which was prevented with CD4
31 ent down-regulation of both IkappaBalpha and IkappaBbeta proteins, derived from a continuous TNF sign
32 These results indicate that IkappaBalpha and IkappaBbeta share significant similarities in their bioc
33 g either stimulus, only the IkappaBalpha and IkappaBbeta steady-state levels declined in parallel wit
34 red divergent properties of IkappaBalpha and IkappaBbeta that influence their ability to activate hep
35 gue hemorrhage and discover IkappaBalpha and IkappaBbeta to be the new cellular targets that are clea
37 ilitated the association of IkappaBalpha and IkappaBbeta with the high molecular weight IKK complex.
38 -kappaB inhibitory proteins IkappaBalpha and IkappaBbeta, resulting in constitutive nuclear expressio
40 e rapid degradation of both IkappaBalpha and IkappaBbeta, two major cytoplasmic inhibitors of NF-kapp
41 related IkappaB molecules, IkappaBalpha and IkappaBbeta, we generated knock-in mice by replacing the
42 two members of the family, IkappaBalpha and IkappaBbeta, which also function in the nucleus to termi
43 led by the IkappaB proteins IkappaBalpha and IkappaBbeta, which restrict NF-kappaB in the cytoplasm a
62 anscript and protein levels of p50, p65, and IkappaBbeta remained relatively unchanged during the cou
63 of NF-kappaB1, NF-kappaB2, RelA, c-Rel, and IkappaBbeta similar to those of wild-type fibroblasts.
65 educed, but not nearly to the same extent as IkappaBbeta, thus highlighting the degree to which Ikapp
68 uctural studies, which predicted that binary IkappaBbeta x NF-kappaB complexes should be capable of n
70 pitation show that NFkappaB/Rel factor-bound IkappaBbeta forms a ternary complex with Cn under in vit
72 link the innate immune response mediated by IkappaBbeta/NF-kappaB to ET-1 expression and potentially
73 tivated HIV in both U1 and J-Lat 10.6 cells, IkappaBbeta knockdown did not activate HIV, and, surpris
75 decreased NF-kappaB activity and concomitant IkappaBbeta accumulation and that these defects were ame
77 nuclear localization signal clearly contacts IkappaBbeta, whereas a homologous segment from the secon
80 rrelated with a reduced level of cytoplasmic IkappaBbeta and could be associated with the overexpress
84 ay in oncogenic transformation, we expressed IkappaBbeta, a specific inhibitor of NF-kappaB, in two h
87 on of NF-kappaB activation that results from IkappaBbeta degradation preserves the enhanced antioxida
89 appaB proteins are significantly homologous, IkappaBbeta contains a unique 47-amino acid insertion of
91 revious observations that hypophosphorylated IkappaBbeta.NF-kappaB complexes can reside in the nucleu
93 h the absence of nuclear, hypophosphorylated-IkappaBbeta bound to p65:c-Rel heterodimers at a specifi
94 e-linked immunosorbent assays; IkappaBalpha, IkappaBbeta, and p105 immunoblot analysis; and nuclear f
95 rs: the prototypical IkappaBs (IkappaBalpha, IkappaBbeta, and IkappaBepsilon), which form low-molecul
97 isappearance of immunoreactive IkappaBalpha, IkappaBbeta, IkappaBgamma, or IkappaBepsilon or with the
98 y related inhibitors including IkappaBalpha, IkappaBbeta, and IkappaBepsilon, which trap NF-kappaB in
99 nucleus secondary to increased IkappaBalpha, IkappaBbeta, and IkappaBepsilon degradation, a mechanism
100 TCR/CD28 costimulation induces IkappaBalpha, IkappaBbeta, and IkappaBepsilon degradation, and PKC is
101 kappaB cytoplasmic inhibitors, IkappaBalpha, IkappaBbeta, and IkappaBepsilon, by these kinases trigge
105 of the Bcl-3-related molecules IkappaBalpha, IkappaBbeta, and IkappaBepsilon in SEB-activated T cells
107 he IkappaB inhibitory subunits IkappaBalpha, IkappaBbeta, and p105; however, following either stimulu
108 Here we show that, unlike IkappaBalpha, IkappaBbeta and IkappaBepsilon appear to sequester p65 o
111 Substitutions of the homologous sites in IkappaBbeta, serines 19 and 23, also prevent inducible I
118 hat NF-kappaB : IkappaBalpha and NF-kappaB : IkappaBbeta complexes are regulated by different upstrea
120 nucleocytoplasmic complex, whereas NF-kappaB.IkappaBbeta complexes are localized to the cytoplasm of
122 proteins are associated only with NF-kappaB:IkappaBbeta complexes and therefore may provide an expla
123 h p65 and c-Rel, and the DNA-bound NF-kappaB:IkappaBbeta complexes are resistant to IkappaBalpha, sug
126 was associated with elevated levels of lung IkappaBbeta (but not IkappaBalpha) protein in the absenc
127 ugh IkappaBalpha and another IkappaB member, IkappaBbeta, can enter the nucleus and repress NF-kappaB
128 ith a plasmid containing cDNA encoding mouse IkappaBbeta, an inhibitor of NF-kappaB, resulted in incr
132 ly, a complex between NF-kappaB and a mutant IkappaBbeta protein containing four serine to alanine mu
134 ces the degradation of IkappaBalpha, but not IkappaBbeta nor an N-terminal deletion mutant of IkappaB
135 the ankyrin repeats of IkappaBalpha, but not IkappaBbeta, contained information necessary for PIR deg
136 hat the specificity of IkappaBalpha, but not IkappaBbeta, to properly regulate NF-kappaB induction du
138 of cRel-containing NF-kappaB dimers, nuclear IkappaBbeta stabilizes NF-kappaB/DNA binding and enhance
139 aB p65 homodimer suggest a model for nuclear IkappaBbeta.NF-kappaB.DNA ternary complex formation.
140 lpha, suggesting hypophosphorylated, nuclear IkappaBbeta may prolong the expression of certain genes.
141 verexpress IkappaBbeta, we show that nuclear IkappaBbeta is both necessary and sufficient to drive LP
144 Like IkappaBalpha, Tax-mediated breakdown of IkappaBbeta in transfected T lymphocytes is blocked eith
145 e findings, we propose that tight control of IkappaBbeta protein by p65 is necessary for the maintena
146 of IkappaBalpha and a sustained decrease of IkappaBbeta that correlated with increased and persisten
148 bited the cytoplasmic protein degradation of IkappaBbeta and IkappaBalpha, as well as repressed their
149 ween the proteasome-dependent degradation of IkappaBbeta and the AICD that occurs through activation
150 A through phosphorylation and degradation of IkappaBbeta and the re-expression of NF-kappaB regulated
152 of NF-kappaB/Rel by promoting degradation of IkappaBbeta as well as enhancing degradation of IkappaBa
154 hosphorylation and subsequent degradation of IkappaBbeta in both human Jurkat T cells and the murine
155 e revealed that the inducible degradation of IkappaBbeta induced by calyculin A, and TNF-alpha requir
157 The calyculin A-mediated degradation of IkappaBbeta is further enhanced by the cytokine tumor ne
158 duced by phorbol ester alone, degradation of IkappaBbeta is largely dependent on the CD28 costimulato
159 served with IkappaBalpha, the degradation Of IkappaBbeta is not associated with its rapid resynthesis
161 onstrate that Tax induces the degradation Of IkappaBbeta, another NF-kappaB/Rel cytoplasmic inhibitor
162 in) in the ubiquitination and degradation of IkappaBbeta, one of the two major IkappaB isoforms in ma
163 tory factor 3 (IRF3) but also degradation of IkappaBbeta, thereby inhibiting IRF3 and NF-kappaB activ
170 at T cells leads to the gradual depletion of IkappaBbeta, which is correlated with the induction of c
175 lly, we have characterized the expression of IkappaBbeta in testis, a tissue in which IkappaBalpha is
179 xpression of a proteolysis-resistant form of IkappaBbeta, but not IkappaBalpha, causes a severe growt
183 could induce anchorage-independent growth of IkappaBbeta-expressing A549 cells, suggesting that the I
184 es suggest that Tax-mediated inactivation Of IkappaBbeta may play a role in the persistent nuclear ex
187 ppaBalpha degradation and the lower level of IkappaBbeta turnover during the second phase of the acti
188 s containing Tax had extremely low levels of IkappaBbeta, but not IkappaBalpha, and contained predomi
190 ibited by an N-terminal truncation mutant of IkappaBbeta that is incapable of responding to the degra
192 able proteasome inhibitors or by mutation Of IkappaBbeta at two serine residues present within its N-
195 have identified a hypophosphorylated pool of IkappaBbeta that shields nuclear NF-kappaB from inhibiti
197 Moreover, swapping the N-terminal region of IkappaBbeta for the corresponding IkappaBalpha sequence
201 esent a necessary but not sufficient role of IkappaBbeta in preventing oxidant stress-induced cell de
203 acid, serine, and threonine-rich sequence of IkappaBbeta in proper localization of IkappaBbeta x NF-k
204 that both the N- and C-terminal sequences of IkappaBbeta are required for the inducible degradation o
205 sults suggest that the degradation signal of IkappaBbeta may be controlled by the opposing actions of
211 TrCP is also necessary for ubiquitination of IkappaBbeta upon stimulation of cells, and deletion of t
213 Moreover, overexpression of IkappaBalpha or IkappaBbeta protects endothelial cells from DENV-induced
214 f IkappaBepsilon, but not of IkappaBalpha or IkappaBbeta, are dramatically reduced upon the stimulati
216 as mice genetically modified to overexpress IkappaBbeta, we show that nuclear IkappaBbeta is both ne
217 tosis was observed in WT MEFs overexpressing IkappaBbeta with simultaneous IkappaBalpha knockdown, wh
220 rmacologic therapies to specifically prevent IkappaBbeta/NF-kappaB signaling, as well as mice genetic
221 hough the abundance of the inhibitor protein IkappaBbeta was higher in 267B1/Ki-ras cells than in 267
226 Deletion of the IkappaBbeta insert renders IkappaBbeta x NF-kappaB complexes capable of shuttling b
230 is based on the ability of p65 to stabilize IkappaBbeta protein from the 26S proteasome, a process m
232 xpress IkappaBalpha, but express a T7-tagged IkappaBbeta under the promoter and regulatory sequence o
236 Using p65(-/-) fibroblasts, we show that IkappaBbeta is profoundly reduced in these cells, but no
237 aced with the IkappaBbeta cDNA, we show that IkappaBbeta overexpression prevented oxidative stress-in
241 whereas MEKK2 participates in assembling the IkappaBbeta:NF-kappaB/IKK complex; these two distinct co
242 nd differences in the mode of binding at the IkappaBbeta sixth ankyrin repeat and NF-kappaB p65 homod
243 ich the IkappaBalpha gene is replaced by the IkappaBbeta cDNA, have uncovered divergent properties of
245 of two basal phosphoacceptors present in the IkappaBbeta PEST domain (Ser-313 and Ser-315) yields a m
246 In this study, we assess the role of the IkappaBbeta insert in regulating cytoplasmic retention o
251 h the IkappaBalpha gene is replaced with the IkappaBbeta cDNA, we show that IkappaBbeta overexpressio
253 G-protein, kappaB-Ras, participates with the IkappaBbeta insert to effectively mask the NF-kappaB nuc
254 multiple Sox binding sites found within the IkappaBbeta promoter and can enhance transcription of a
256 growth, whereas NF-kappaB signaling through IkappaBbeta degradation mediated apoptosis and P-selecti
258 on experiments revealed that, in addition to IkappaBbeta, other IkappaB family members examined (p105
259 e functional fate of NF-kappaB when bound to IkappaBbeta is critically dependent on the phosphorylati
260 on in vivo, whereas replacement of these two IkappaBbeta residues with a phosphoserine mimetic genera
264 etween the strong Ikappa Balpha and the weak IkappaBbeta inhibitors switches their in vivo inhibitory
265 ed by a selective IKKbeta inhibitor, whereas IkappaBbeta degradation was attenuated, suggesting a mec
266 simultaneous IkappaBalpha knockdown, whereas IkappaBbeta overexpression alone did not produce this ef
267 s shuttle in and out of the nucleus, whereas IkappaBbeta x NF-kappaB complexes are retained exclusive
268 turn-off of the NF-kappaB response, whereas IkappaBbeta and - epsilon function to reduce the system'
271 ive cells c-Rel is associated primarily with IkappaBbeta, an inhibitory molecule that is not effectiv
272 e that beta-TrCP interacts specifically with IkappaBbeta, and such interaction is dependent on prior
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