Journal ArticleDOI
The role of NF-κB in the regulation of cell stress responses
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TLDR
The purpose of this review is to briefly summarize the recent progress in the studies of the role of reactive oxygen species, cytokines and ionizing radiation in NF-kappaB activation.About:
This article is published in International Immunopharmacology.The article was published on 2002-10-01. It has received 295 citations till now. The article focuses on the topics: Effector & Cell activation.read more
Citations
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Molecular and evolutionary basis of the cellular stress response
TL;DR: Functional analysis of the minimal stress proteome yields information about key aspects of the cellular stress response, including physiological mechanisms of sensing membrane lipid, protein, and DNA damage; redox sensing and regulation; cell cycle control; macromolecular stabilization/repair; and control of energy metabolism.
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Reactive oxygen species in tumor progression.
TL;DR: The finding that a diet rich in antioxidants or the elimination of ROS by antioxidant compounds prevents the development of certain cancers provided the setting for subsequent investigation of the tumorigenic actions of reactive oxygen species.
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Mitochondrial signaling in mammalian cells activated by red and near-IR radiation.
TL;DR: The present review examines the question whether radiation of visible and near‐IR (IR‐A) radiation can activate this retrograde‐type cellular signaling pathway and functions of cytochrome c oxidase as a signal generator and a signal transducer in irradiated cells.
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Anticancer activity of metal complexes: involvement of redox processes.
Ute Jungwirth,Christian R. Kowol,Bernhard K. Keppler,Christian G. Hartinger,Walter Berger,Petra Heffeter +5 more
TL;DR: The aim of this review is to highlight specific interactions of metal-based anticancer drugs with the cellular redox homeostasis and to explain this behavior by considering chemical properties of the respective anticancer metal complexes currently either in (pre)clinical development or in daily clinical routine in oncology.
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Proposed mechanisms for the induction of insulin resistance by oxidative stress.
Asnat Bloch-Damti,Nava Bashan +1 more
TL;DR: Administration of antioxidants such as lipoic acid in oxidized cells, in animal models of diabetes, and in type 2 diabetes shows improved insulin sensitivity, and oxidative stress is presently accepted as a likely causative factor in the development of insulin resistance.
References
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Journal ArticleDOI
Function and activation of NF-kappa B in the immune system.
TL;DR: The inhibition of NF-kappa B activation by antioxidants and specific protease inhibitors may provide a pharmacological basis for interfering with these acute processes in suppressing toxic/septic shock, graft-vs-host reactions, acute inflammatory reactions, severe phase response, and radiation damage.
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Reactive oxygen intermediates as apparently widely used messengers in the activation of the NF-kappa B transcription factor and HIV-1.
TL;DR: It is shown that micromolar concentrations of H2O2 can induce the expression and replication of HIV‐1 in a human T cell line and suggests that diverse agents thought to activate NF‐kappa B by distinct intracellular pathways might all act through a common mechanism involving the synthesis of ROI.
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NF-κB: Ten Years After
TL;DR: The manuscript and the Figures and Table are based on a manuscript originally written by Gordon C. Dickinson in 2012 and then edited by David I. Dickinson and revised by David A. Dickinson.
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Transcriptional activation by tetracyclines in mammalian cells
Manfred Gossen,Sabine Freundlieb,Gabriele Bender,Gerhard Müller,Wolfgang Hillen,Hermann Bujard +5 more
TL;DR: Adding doxycycline to HeLa cells that constitutively synthesized the transactivator and that contained an appropriate, stably integrated reporter unit rapidly induced gene expression more than a thousandfold.
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TNF- and Cancer Therapy-Induced Apoptosis: Potentiation by Inhibition of NF-κB
TL;DR: The activation of the transcription factor nuclear factor-kappa B by tumor necrosis factor, ionizing radiation, or daunorubicin, was found to protect from cell killing, providing a mechanism of cellular resistance to killing by some apoptotic reagents.