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Open AccessJournal ArticleDOI

Complementation Cloning of NEMO, a Component of the IκB Kinase Complex Essential for NF-κB Activation

TLDR
A flat cellular variant of HTLV-1 Tax-transformed rat fibroblasts, 5R, which is unresponsive to all tested NF-κB activating stimuli is characterized, and its genetic complementation is reported.
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This article is published in Cell.The article was published on 1998-06-26 and is currently open access. It has received 1061 citations till now. The article focuses on the topics: CHUK & IκB kinase.

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Citations
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Innate Immune Recognition

TL;DR: Microbial recognition by Toll-like receptors helps to direct adaptive immune responses to antigens derived from microbial pathogens to distinguish infectious nonself from noninfectious self.
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Phosphorylation meets ubiquitination: the control of NF-[kappa]B activity.

TL;DR: Recent progress has been made in understanding the details of the signaling pathways that regulate NF-kappaB activity, particularly those responding to the proinflammatory cytokines tumor necrosis factor-alpha and interleukin-1.
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Shared principles in NF-kappaB signaling

TL;DR: The authors synthesize some of the basic principles that have emerged from studies of NF-kappaB, and aim to generate a more unified view of the regulation of the transcription factor.
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Signaling to NF-kappaB.

TL;DR: An overview of established NF-kappaB signaling pathways is provided with focus on the current state of research into the mechanisms that regulate IKK activation and NF- kappaB transcriptional activity.
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NF-κB: a key role in inflammatory diseases

TL;DR: The specificity of various NF-κB proteins, their role in inflammatory disease, the regulation of NF-β proteins and IκB activity by IκBs and IkkB kinase, and the development of therapeutic strategies aimed at inhibition are discussed.
References
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THE NF-κB AND IκB PROTEINS: New Discoveries and Insights

TL;DR: The transcription factor NF-κB has attracted widespread attention among researchers in many fields based on its unusual and rapid regulation, the wide range of genes that it controls, its central role in immunological processes, the complexity of its subunits, and its apparent involvement in several diseases.
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Jak-STAT pathways and transcriptional activation in response to IFNs and other extracellular signaling proteins

TL;DR: A previously unrecognized direct signal transduction pathway to the nucleus has been uncovered: IFN-receptor interaction at the cell surface leads to the activation of kinases of the Jak family that phosphorylate substrate proteins called STATs (signal transducers and activators of transcription).
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A cytokine-responsive IκB kinase that activates the transcription factor NF-κB

TL;DR: IKK turns out to be the long-sought-after protein kinase that mediates the critical regulatory step in NF-κB activation, and phosphorylates IκBs on the sites that trigger their degradation.
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IKK-1 and IKK-2: Cytokine-Activated IκB Kinases Essential for NF-κB Activation

TL;DR: In this article, a large multiprotein complex, the IkappaB kinase (IKK) signalsome, was purified from HeLa cells and found to contain a cytokine-inducible IKK kinase activity that phosphorylates IappaB-alpha and IKK-beta.
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Suppression of human colorectal carcinoma cell growth by wild-type p53.

TL;DR: It is shown that the wild-type gene can specifically suppress the growth of human colorectal carcinoma cells in vitro and that an in vivo-derived mutation resulting in a single conservative amino acid substitution in the p53 gene product abrogates this suppressive ability.
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