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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 ed in substrates of canonical (IkappaBalpha, IkappaBbeta) and alternative (p100) NF-kappaB pathways,
96 rs: the prototypical IkappaBs (IkappaBalpha, IkappaBbeta, and IkappaBepsilon), which form low-molecul
98 isappearance of immunoreactive IkappaBalpha, IkappaBbeta, IkappaBgamma, or IkappaBepsilon or with the
99 y related inhibitors including IkappaBalpha, IkappaBbeta, and IkappaBepsilon, which trap NF-kappaB in
100 nucleus secondary to increased IkappaBalpha, IkappaBbeta, and IkappaBepsilon degradation, a mechanism
101 TCR/CD28 costimulation induces IkappaBalpha, IkappaBbeta, and IkappaBepsilon degradation, and PKC is
102 kappaB cytoplasmic inhibitors, IkappaBalpha, IkappaBbeta, and IkappaBepsilon, by these kinases trigge
106 of the Bcl-3-related molecules IkappaBalpha, IkappaBbeta, and IkappaBepsilon in SEB-activated T cells
108 he IkappaB inhibitory subunits IkappaBalpha, IkappaBbeta, and p105; however, following either stimulu
109 Here we show that, unlike IkappaBalpha, IkappaBbeta and IkappaBepsilon appear to sequester p65 o
112 Substitutions of the homologous sites in IkappaBbeta, serines 19 and 23, also prevent inducible I
119 hat NF-kappaB : IkappaBalpha and NF-kappaB : IkappaBbeta complexes are regulated by different upstrea
121 nucleocytoplasmic complex, whereas NF-kappaB.IkappaBbeta complexes are localized to the cytoplasm of
123 proteins are associated only with NF-kappaB:IkappaBbeta complexes and therefore may provide an expla
124 h p65 and c-Rel, and the DNA-bound NF-kappaB:IkappaBbeta complexes are resistant to IkappaBalpha, sug
127 was associated with elevated levels of lung IkappaBbeta (but not IkappaBalpha) protein in the absenc
128 ugh IkappaBalpha and another IkappaB member, IkappaBbeta, can enter the nucleus and repress NF-kappaB
129 ith a plasmid containing cDNA encoding mouse IkappaBbeta, an inhibitor of NF-kappaB, resulted in incr
133 ly, a complex between NF-kappaB and a mutant IkappaBbeta protein containing four serine to alanine mu
135 ces the degradation of IkappaBalpha, but not IkappaBbeta nor an N-terminal deletion mutant of IkappaB
136 the ankyrin repeats of IkappaBalpha, but not IkappaBbeta, contained information necessary for PIR deg
137 hat the specificity of IkappaBalpha, but not IkappaBbeta, to properly regulate NF-kappaB induction du
139 of cRel-containing NF-kappaB dimers, nuclear IkappaBbeta stabilizes NF-kappaB/DNA binding and enhance
140 aB p65 homodimer suggest a model for nuclear IkappaBbeta.NF-kappaB.DNA ternary complex formation.
141 lpha, suggesting hypophosphorylated, nuclear IkappaBbeta may prolong the expression of certain genes.
142 verexpress IkappaBbeta, we show that nuclear IkappaBbeta is both necessary and sufficient to drive LP
145 Like IkappaBalpha, Tax-mediated breakdown of IkappaBbeta in transfected T lymphocytes is blocked eith
146 e findings, we propose that tight control of IkappaBbeta protein by p65 is necessary for the maintena
147 of IkappaBalpha and a sustained decrease of IkappaBbeta that correlated with increased and persisten
149 bited the cytoplasmic protein degradation of IkappaBbeta and IkappaBalpha, as well as repressed their
150 ween the proteasome-dependent degradation of IkappaBbeta and the AICD that occurs through activation
151 A through phosphorylation and degradation of IkappaBbeta and the re-expression of NF-kappaB regulated
153 of NF-kappaB/Rel by promoting degradation of IkappaBbeta as well as enhancing degradation of IkappaBa
155 hosphorylation and subsequent degradation of IkappaBbeta in both human Jurkat T cells and the murine
156 e revealed that the inducible degradation of IkappaBbeta induced by calyculin A, and TNF-alpha requir
158 The calyculin A-mediated degradation of IkappaBbeta is further enhanced by the cytokine tumor ne
159 duced by phorbol ester alone, degradation of IkappaBbeta is largely dependent on the CD28 costimulato
160 served with IkappaBalpha, the degradation Of IkappaBbeta is not associated with its rapid resynthesis
162 onstrate that Tax induces the degradation Of IkappaBbeta, another NF-kappaB/Rel cytoplasmic inhibitor
163 in) in the ubiquitination and degradation of IkappaBbeta, one of the two major IkappaB isoforms in ma
164 tory factor 3 (IRF3) but also degradation of IkappaBbeta, thereby inhibiting IRF3 and NF-kappaB activ
171 at T cells leads to the gradual depletion of IkappaBbeta, which is correlated with the induction of c
176 lly, we have characterized the expression of IkappaBbeta in testis, a tissue in which IkappaBalpha is
180 xpression of a proteolysis-resistant form of IkappaBbeta, but not IkappaBalpha, causes a severe growt
184 could induce anchorage-independent growth of IkappaBbeta-expressing A549 cells, suggesting that the I
185 es suggest that Tax-mediated inactivation Of IkappaBbeta may play a role in the persistent nuclear ex
188 ppaBalpha degradation and the lower level of IkappaBbeta turnover during the second phase of the acti
189 s containing Tax had extremely low levels of IkappaBbeta, but not IkappaBalpha, and contained predomi
191 ibited by an N-terminal truncation mutant of IkappaBbeta that is incapable of responding to the degra
193 able proteasome inhibitors or by mutation Of IkappaBbeta at two serine residues present within its N-
196 have identified a hypophosphorylated pool of IkappaBbeta that shields nuclear NF-kappaB from inhibiti
198 Moreover, swapping the N-terminal region of IkappaBbeta for the corresponding IkappaBalpha sequence
202 esent a necessary but not sufficient role of IkappaBbeta in preventing oxidant stress-induced cell de
204 acid, serine, and threonine-rich sequence of IkappaBbeta in proper localization of IkappaBbeta x NF-k
205 that both the N- and C-terminal sequences of IkappaBbeta are required for the inducible degradation o
206 sults suggest that the degradation signal of IkappaBbeta may be controlled by the opposing actions of
212 TrCP is also necessary for ubiquitination of IkappaBbeta upon stimulation of cells, and deletion of t
214 Moreover, overexpression of IkappaBalpha or IkappaBbeta protects endothelial cells from DENV-induced
215 f IkappaBepsilon, but not of IkappaBalpha or IkappaBbeta, are dramatically reduced upon the stimulati
217 as mice genetically modified to overexpress IkappaBbeta, we show that nuclear IkappaBbeta is both ne
218 tosis was observed in WT MEFs overexpressing IkappaBbeta with simultaneous IkappaBalpha knockdown, wh
221 rmacologic therapies to specifically prevent IkappaBbeta/NF-kappaB signaling, as well as mice genetic
222 hough the abundance of the inhibitor protein IkappaBbeta was higher in 267B1/Ki-ras cells than in 267
227 Deletion of the IkappaBbeta insert renders IkappaBbeta x NF-kappaB complexes capable of shuttling b
231 is based on the ability of p65 to stabilize IkappaBbeta protein from the 26S proteasome, a process m
233 xpress IkappaBalpha, but express a T7-tagged IkappaBbeta under the promoter and regulatory sequence o
237 Using p65(-/-) fibroblasts, we show that IkappaBbeta is profoundly reduced in these cells, but no
238 aced with the IkappaBbeta cDNA, we show that IkappaBbeta overexpression prevented oxidative stress-in
242 whereas MEKK2 participates in assembling the IkappaBbeta:NF-kappaB/IKK complex; these two distinct co
243 nd differences in the mode of binding at the IkappaBbeta sixth ankyrin repeat and NF-kappaB p65 homod
244 ich the IkappaBalpha gene is replaced by the IkappaBbeta cDNA, have uncovered divergent properties of
246 of two basal phosphoacceptors present in the IkappaBbeta PEST domain (Ser-313 and Ser-315) yields a m
247 In this study, we assess the role of the IkappaBbeta insert in regulating cytoplasmic retention o
252 h the IkappaBalpha gene is replaced with the IkappaBbeta cDNA, we show that IkappaBbeta overexpressio
254 G-protein, kappaB-Ras, participates with the IkappaBbeta insert to effectively mask the NF-kappaB nuc
255 multiple Sox binding sites found within the IkappaBbeta promoter and can enhance transcription of a
257 growth, whereas NF-kappaB signaling through IkappaBbeta degradation mediated apoptosis and P-selecti
259 on experiments revealed that, in addition to IkappaBbeta, other IkappaB family members examined (p105
260 e functional fate of NF-kappaB when bound to IkappaBbeta is critically dependent on the phosphorylati
261 on in vivo, whereas replacement of these two IkappaBbeta residues with a phosphoserine mimetic genera
265 etween the strong Ikappa Balpha and the weak IkappaBbeta inhibitors switches their in vivo inhibitory
266 ed by a selective IKKbeta inhibitor, whereas IkappaBbeta degradation was attenuated, suggesting a mec
267 simultaneous IkappaBalpha knockdown, whereas IkappaBbeta overexpression alone did not produce this ef
268 s shuttle in and out of the nucleus, whereas IkappaBbeta x NF-kappaB complexes are retained exclusive
269 turn-off of the NF-kappaB response, whereas IkappaBbeta and - epsilon function to reduce the system'
272 ive cells c-Rel is associated primarily with IkappaBbeta, an inhibitory molecule that is not effectiv
273 e that beta-TrCP interacts specifically with IkappaBbeta, and such interaction is dependent on prior