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• W1915074145 endingPage "2818" @default.
• W1915074145 startingPage "2809" @default.
• W1915074145 abstract "The eukaryotic transcription factor NF-kappa B plays a central role in the induced expression of human immunodeficiency virus type 1 and in many aspects of the genetic program mediating normal T-cell activation and growth. The nuclear activity of NF-kappa B is tightly regulated from the cytoplasmic compartment by an inhibitory subunit called I kappa B alpha. This cytoplasmic inhibitor is rapidly phosphorylated and degraded in response to a diverse set of NF-kappa B-inducing agents, including T-cell mitogens, proinflammatory cytokines, and viral transactivators such as the Tax protein of human T-cell leukemia virus type 1. To explore these I kappa B alpha-dependent mechanisms for NF-kappa B induction, we identified novel mutants of I kappa B alpha that uncouple its inhibitory and signal-transducing functions in human T lymphocytes. Specifically, removal of the N-terminal 36 amino acids of I kappa B alpha failed to disrupt its ability to form latent complexes with NF-kappa B in the cytoplasm. However, this deletion mutation prevented the induced phosphorylation, degradative loss, and functional release of I kappa B alpha from NF-kappa B in Tax-expressing cells. Alanine substitutions introduced at two serine residues positioned within this N-terminal regulatory region of I kappa B alpha also yielded constitutive repressors that escaped from Tax-induced turnover and that potently inhibited immune activation pathways for NF-kappa B induction, including those initiated from antigen and cytokine receptors. In contrast, introduction of a phosphoserine mimetic at these sites rectified this functional defect, a finding consistent with a causal linkage between the phosphorylation status and proteolytic stability of this cytoplasmic inhibitor. Together, these in vivo studies define a critical signal response domain in I kappa B alpha that coordinately controls the biologic activities of I kappa B alpha and NF-kappa B in response to viral and immune stimuli." @default.
• W1915074145 created "2016-06-24" @default.
• W1915074145 creator A5010426134 @default.
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• W1915074145 date "1995-05-01" @default.
• W1915074145 modified "2023-10-10" @default.
• W1915074145 title "Coupling of a Signal Response Domain in IκBα to Multiple Pathways for NF-κB Activation" @default.
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• W1915074145 doi "https://doi.org/10.1128/mcb.15.5.2809" @default.
• W1915074145 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/230512" @default.
• W1915074145 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/7739562" @default.
• W1915074145 hasPublicationYear "1995" @default.
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