The peroxiredoxin family was discovered approximately 30 years ago and is now recognized as one of the most important families of enzymes related to antioxidant defense and cellular signaling. Peroxiredoxin 6 shares the basic enzymatic functions that characterize this family, but also exhibits several unique and crucial activities. These include the ability to reduce phospholipid hydroperoxides, phospholipase A2 activity, and an acyl transferase activity that is important in phospholipid remodeling. This book describes the available models for investigating the unique functions of PRDX6 and its role in normal physiological function, as well its roles in the pathophysiology of diseases including cancer, diseases of the eye, and male fertility.

This book contains a broad survey on the peroxiredoxins. It involves almost all groups that contributed significant insights into the emerging field. Coverage discusses the diverse biological roles of the new protein family in the context of other antioxidant systems like those based on heme or selenium catalysis. In addition, the book highlights related future perspectives.

Redox Chemistry and Biology of Thiols offers an applied, comprehensive overview of redox chemistry and biology of thiol-dependent processes. Running from basic biology and chemistry of redox phenomena to research methods and highlighting recently identified roles of thiols across cellular and bodily systems, this book draws upon a range of disciplines to illuminate new research directions, new applications of thiol studies, and clinical translation. Sections cover thiol oxidizing species, thiol reactivity and modifications, thioredoxin, glutaredoxin, glutathione, peroxidases, thiol repair enzymes, thiol oxidative signaling, disulfide bond formation, thiol-based redox biosensors, cysteine and hydrogen sulfide metabolism, iron-sulfur cluster biogenesis, thiols in chloroplasts, blood thiols, sugar and polyamine thiols in pathogenic organisms, redox medicine (therapeutic applications of thiols and drug development), as well as methods and bioinformatics tools. - Runs from basic thiol biology and chemistry to applications and clinical translation - Provides methods and protocols that will power new research across biomedicine, cell biology, plant biology, drug development, and protein folding and modulation - Includes chapter contributions from international leaders in the field

This book provides an overview of antioxidants and antioxidant enzymes and their role in the mechanisms of signaling and cellular tolerance under stress in plant systems. Major reactive oxygen species (ROS)-scavenging/modulating enzymes include the superoxide dismutase (SOD) that dismutates O2 into H2O2, which is followed by the coordinated action of a set of enzymes including catalase (CAT), ascorbate peroxidase (APX), glutathione peroxidase (GPX) and peroxiredoxins (Prx) that remove H2O2. In addition to the ROS scavenging enzymes, a number of other enzymes are found in various subcellular compartments, which are involved in maintaining such redox homeostasis either by directly scavenging particular ROS and ROS-byproducts or by replenishing antioxidants. In that respect, these enzymes can be also considered antioxidants. Such enzymes include monodehydroascorbate reductase (MDAR), dehydroascorbate reductase (DHAR), glutathione reductase (GR), alternative oxidases (AOXs), peroxidases (PODs) and glutathione S-transferases (GSTs). Some non-enzymatic antioxidants, such as ascorbic acid (vitamin C), carotenes (provitamin A), tocopherols (vitamin E), and glutathione (GSH), work in concert with antioxidant enzymes to sustain an intracellular steady-state level of ROS that promotes plant growth, development, cell cycles and hormone signaling, and reinforces the responses to abiotic and biotic environmental stressors. Offering a unique compilation of information on antioxidants and antioxidant enzymes, this is a valuable resource for advanced students and researchers working on plant biochemistry, physiology, biotechnology, and signaling in cell organelles, and those specializing in plant enzyme technology.

Biological processes are driven by complex systems of functionally interacting signaling molecules. Thus, understanding signaling molecules is essential to explain normal or pathological biological phenomena. A large body of clinical and experimental data has been accumulated over these years, albeit in fragmented state. Hence, systems biological approaches concomitant with the understanding of each molecule are ideal to delineate signaling networks/pathways involved in the biologically important processes. The control of these signaling pathways will enrich our healthier life. Currently, there are more than 30,000 genes in human genome. However, not all the proteins encoded by these genes work equally in order to maintain homeostasis. Understanding the important signaling molecules as completely as possible will significantly improve our research-based teaching and scientific capabilities. This encyclopedia presents 350 biologically important signaling molecules and the content is built on the core concepts of their functions along with early findings written by some of the world’s foremost experts. The molecules are described by recognized leaders in each molecule. The interactions of these single molecules in signal transduction networks will also be explored. This encyclopedia marks a new era in overview of current cellular signaling molecules for the specialist and the interested non-specialist alike During past years, there were multiple databases to gather this information briefly and very partially. Amidst the excitement of these findings, one of the great scientific tasks of the coming century is to bring all the useful information into a place. Such an approach is arduous but at the end will infuse the lacunas and considerably be a streamline in the understanding of vibrant signaling networks. Based on this easy-approach, we can build up more complicated biological systems.

Brain disorders, including neurological and neuropsychiatric conditions, represent a challenge for public health systems and society at large. The limited knowledge of their biology hampers the development of diagnostic tools and effective therapeutics. A clear understanding of the mechanisms that underlie the onset and progression of brain disorders is required in order to identify new avenues for therapeutic intervention. Overlapping genetic risk factors across different brain disorders suggest common linkages and pathophysiological mechanisms that underlie brain disorders. Methodological and technological advances are leading to new insights that go beyond traditional hypotheses. Taking account of underlying molecular, cellular and systems biology underlying brain function will play an important role in the classification of brain disorders in future. In this Research Topic, the latest advances in our understanding of biological mechanisms across different brain disorders are presented. The areas covered include developments in neurogenetics, epigenetics, plasticity, glial cell biology, neuroimmune interactions and new technologies associated with the study of brain function. Examples of how understanding of biological mechanisms are translating into research strategies that aim to advance diagnoses and treatment of brain disorders are discussed.

When we worked on Down Syndrome brain in the past we have been focus ing on adult brain. This was a major step forwards as most work on Down Syndrome was carried out on fibroblasts or other tissues and, moreover, we introduced proteomics to identify and quantify brain protein expression. We considered evaluation of brain protein expression in Down Syndrome brain by and by more important than gene hunting at the nucleic acid level realiz ing the long unpredictable way from RNA to protein. The availability of fetal samples along with the proteomic appproach stimulated and reinforced studies on Down Syndrome brain. And indeed, it was found out that some observations on aberrant protein expression in adult Down Syndrome brain could not be verified in the fetal samples indi cating that neurodegeneration in adult Down Syndrome brain may have been responsible rather than trisomy 21. Using brains from the early second trimester of gestation led to the generation of a series of clues for the under standing of aberrant wiring of the brain in Down Syndrome and enabled the determination of altered key functions in early life; e. g. undetectably low drebrin was observed in Down Syndrome cortex, an integral constituent and marker for dendritic spines, main effectors of cross-talk between neurons. In addition, evaluation of the nature of the neuronal deficits in terms of neuro transmission markers could be established as well as neuronal density in fetal Down Syndrome cortex.