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IkappaBbeta has essential functions within the Rel-NFkappaB generation module, specifically for the RelA:RelA homodimer, which controls a subset of NFkappaB target genes.
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these results mechanistically link the innate immune response mediated by IkappaBbeta/NF-kappaB to ET-1 expression and potentially reveal therapeutic targets for patients with Gram-negative septic shock.
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Dengue virus protease interacts with both IkappaBalpha and IkappaBbeta cleaving them in a mouse hemorrhage model.
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sustained NF-kappaB activity mediated by IkappaBbeta protects against hyperoxic lung injury through increased expression of antiapoptotic genes
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Findings represent a necessary but not sufficient role of IkappaBbeta in preventing oxidant stress-induced cell death.
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IkappaBbeta is an essential co-activator for LPS-induced IL-1beta transcription in vivo.
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IkappaBbeta acts through p65:c-Rel dimers to maintain prolonged expression of TNF-alpha
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data suggest that RelA is liberated during LPS-induced pulmonary inflammation by the regulated degradation of both IkappaB-alpha and IkappaB-beta
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temporal control of NF-kappaB activation by the coordinated degradation and synthesis of IkappaB proteins
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beta-TrCP1 contributes to, but is not absolutely required for, the degradation of I kappa B and beta-catenin
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controls osteoclatogenesis
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Direct administration of dominant negative I-kappa B or tyrosine 42-mutated I-kappa B proteins before induction of inflammatory arthritis attenuates in vivo activation of NF-kappa B and blocks joint swelling, osteoclast recruitment, and osteolysis.
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IkappaBalpha and IkappaBbeta play unique injury context-specific roles in activating NF-kappaB-mediated proinflammatory responses
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activation required for HSV-1 efficient replication
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Results suggest that tight control of IkappaBbeta protein by p65 is necessary for the maintenance of cellular homeostasis.
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In vivo degradation rate constants were measured for NF-kappaB-bound & -unbound IkappaB. Models suggest differential degradation rates of free & bound IkappaB may be a new cross-regulation mechanism imparting functional robustness to the signaling module.
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These results show that mitochondrial stress signaling uses an IkappaBbeta-initiated NFkappaB pathway that is distinct from the other known NFkappaB pathways.