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NF-kappa B and Rel proteins: evolutionarily conserved mediators of immune responses.
Recently, significant advances have been made in elucidating the details of the pathways through which signals are transmitted to the NF-kappa B:I kappa B complex in the cytosol and their implications for the study of NF-Kappa B.
Phosphorylation of NF-kappa B p65 by PKA stimulates transcriptional activity by promoting a novel bivalent interaction with the coactivator CBP/p300.
MyD88 is an adaptor protein in the hToll/IL-1 receptor family signaling pathways.
Inhibition of NF-kappa B by sodium salicylate and aspirin.
The anti-inflammatory drugs sodium salicylate and aspirin inhibited the activation of NF-kappa B, which further explains the mechanism of action of these drugs.
The transcriptional activity of NF-kappaB is regulated by the IkappaB-associated PKAc subunit through a cyclic AMP-independent mechanism.
This pathway represents a novel mechanism for the cAMP-independent activation of PKA and the regulation of NF-kappaB activity and the subsequent phosphorylation of p65 by protein kinase A.
Toll-like receptor-mediated NF-kappaB activation: a phylogenetically conserved paradigm in innate immunity.
The role of the conserved TLR/NF-κB signaling pathway in innate immunity, as well as its impact on adaptive immune responses, is focused on.
Embryonic lethality and liver degeneration in mice lacking the RelA component of NF-kappa B.
Results indicate that RelA controls inducible, but not basal, transcription in NF-kappa B-regulated pathways, and suggest that the latter is a key regulator of genes involved in responses to infection, inflammation and stress.
ECSIT is an evolutionarily conserved intermediate in the Toll/IL-1 signal transduction pathway.
It is suggested that processing of MEKK-1 is required for its function in the Toll/IL-1 pathway and an important role for ECSIT in signaling to NF-kappaB is indicated.
NF-kappaB and the immune response.
The role of the NF-kappaB pathway in the development and functioning of the immune system is described and various aspects of innate and adaptive immune responses are described.
Selective inhibition of NF-kappaB activation by a peptide that blocks the interaction of NEMO with the IkappaB kinase complex.
The NBD provides a target for the development of drugs that would block proinflammatory activation of the IKK complex without inhibiting basal NF-kappaB activity.