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Now in two-colour throughout, the fourth edition of Eukaryotic Transcription Factors has been completely rewritten and restructured to take into account the tremendous advances in our understanding of transcription factors and the mechanisms by which they act. Considerable emphasis has been given to the interaction between transcription factors and chromatin structure. Also included is an entirely new section on the mediator complex and expansion of the space devoted to co-activators and co-repressors.This book is essential reading for all those who wish to understand the impac

Eukaryotic Cells. --- Gene Expression Regulation. --- Transcription Factors. --- Transcription, Genetic. --- Transcription factors. --- Genetic transcription --- Eukaryotic cells. --- Facteurs de transcription --- Transcription génétique --- Cellules eucaryotes --- Regulation. --- Régulation --- Genetic transcription. --- Genetic regulation --- Genetic transcription factors --- Proteins --- Transcription factors --- Eukaryotic cells --- MOLECULAR STRUCTURE --- BASE SEQUENCE --- DNA-BINDING PROTEINS --- GENETIC PREDISPOSITION TO DISEASE --- TRANSCRIPTION, GENETIC --- DNA-DIRECTED RNA POLYMERASES --- CHROMATIN --- TRANSCRIPTION FACTORS --- ULTRASTRUCTURE

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Our common knowledge on oxidative stress has evolved substantially over the years and has been mostly focused on the fundamental chemical reactions and the most relevant chemical species involved in the human pathophysiology of oxidative stress-associated diseases. Thus, reactive oxygen species and reactive nitrogen species (ROS and RNS) were identified as the key players initiating, mediating, and regulating the cellular and biochemical complexity of oxidative stress either as physiological (acting pro-hormetic) or as pathogenic (causing destructive vicious circle) process. The papers published in this particular Special Issue of the Cells demonstrate the impressive pathophysiological relevance of ROS and RNS in a range of contexts, including the relevance of second messengers of free radicals like 4-hydroxynonenal, allowing us to assume that even more detailed mechanisms of their positive and negative effects lie in wait, and should assist in better monitoring of the major modern diseases and the development of advanced integrative biomedicine treatments.

toxicity --- toll-like receptors --- acrolein --- hydroxyapatite-based biomaterials --- LC-MS/MS --- blood–brain barrier --- NADPH-oxidase --- human neuroblastoma SH-SY5Y cells --- NRF2-NQO1 axis --- granulocytes --- free radicals --- antioxidant --- plaque vulnerability --- bEnd.3 --- relaxation --- Ca2+ --- keratinocytes --- oxidative metabolism of the cells --- lipid peroxidation --- intermittent hypoxia --- osteoblast growth --- UV radiation --- ROS --- bEnd5 --- cyclopurines --- NF?B --- glucose deprivation --- antimicrobial --- endothelial cells --- 4-hydroxynonenal (4-HNE) --- histamine --- glutamine deprivation --- optical coherence tomography --- antioxidants --- DNA damage --- glutathione --- NQO1 transcript variants --- xeroderma pigmentosum --- cancer cells --- VAS2870 --- reactive oxygen species (ROS) --- TP53 mutation --- DNA and RNA polymerases --- viability --- oxidative burst --- macrophages --- inflammation --- Nrf2 --- von Willebrand factor --- reactive oxygen species --- growth control --- intracellular signaling --- MFN2 --- nuclear factor erythroid 2–related factor 2 --- fusion/fission --- IMR-90 --- calcium --- proliferation --- mitochondria --- pathophysiology of oxidative stress --- redox balance --- 4-hydroxynonenal --- cannabidiol --- oxidative homeostasis --- rs1800566 --- neuronal cell death --- heme-oxygenase-1 --- vitamins --- cell signaling --- TRPM2 channel --- aorta --- cancer --- growth --- cancer regression --- oxidative stress --- nucleotide excision repair