Chromatin Readers in Health and Disease, Volume 35, a new release in the Translational Epigenetics series, gathers and makes actionable our current understanding of how chromatin readers regulate access to genetic information, and how their aberrant regulation can contribute to human pathologies. Chromatin readers discussed include 14-3-3 Dinshaw, ADD, Ankyrin, BAH, BET, BIR, BRCT, bromodomains and Kac readers, chromodomains and chromobarrel readers, citrullination readers, macrodomains and poly-ADP-ribose readers, MBT, PHD and double PHD, PWWP, SUMO (H4K12) readers, Tudor and TTD, UDR and ubiquitin, WD40, YEATS (crotonyl reader), MBD, SRA, and Methyl-RNA readers.In the book, more than a dozen leaders in the field examine a range of protein readers, their relationship to human disease, and the early therapeutics that act as chromatin signaling factors to treat cancers and Huntington's disease, among other disorders. Enables researchers and clinicians to understand chromatin signaling mechanisms that regulate gene expression through chromatin readers Highlights the role of chromatin readers in a variety of human pathologies, as well as early therapeutics that act on chromatin signaling Includes chapter contributions from international leaders in the field

Chromatin Signaling and Diseases covers the molecular mechanisms that regulate gene expression, which govern everything from embryonic development, growth, and human pathologies associated with aging, such as cancer. This book helps researchers learn about or keep up with the quickly expanding field of chromatin signaling. After reading this book, clinicians will be more capable of explaining the mechanisms of gene expression regulation to their patients to reassure them about new drug developments that target chromatin signaling mechanisms. For example, several epigenetic drugs that act on chromatin signaling factors are in clinical trials or even approved for usage in cancer treatments, Alzheimer's, and Huntington's diseases. Other epigenetic drugs are in development to regulate various class of chromatin signaling factors. To keep up with this changing landscape, clinicians and doctors will need to stay familiar with genetic advances that translate to clinical practice, such as chromatin signaling. Although sequencing of the human genome was completed over a decade ago and its structure investigated for nearly half a century, molecular mechanisms that regulate gene expression remain largely misunderstood. An emerging concept called chromatin signaling proposes that small protein domains recognize chemical modifications on the genome scaffolding histone proteins, facilitating the nucleation of enzymatic complexes at specific loci that then open up or shut down the access to genetic information, thereby regulating gene expression. The addition and removal of chemical modifications on histones, as well as the proteins that specifically recognize these, is reviewed in Chromatin Signaling and Diseases. Finally, the impact of gene expression defects associated with malfunctioning chromatin signaling is also explored. Explains molecular mechanisms that regulate gene expression, which governs everything from embryonic development, growth, and human pathologies associated with aging Educates clinicians and researchers about chromatin signaling, a molecular mechanism that is changing our understanding of human pathology Explores the addition and removal of chemical modifications on histones, the proteins that specifically recognize these, and the impact of gene expression defects associated with malfunctioning chromatin signaling Helps researchers learn about the quickly expanding field of chromatin signaling

​​​​​​​​​​​​​​​​​​​​​​​ Epigenetic modifications underlie all aspects of human physiology, including stem cell renewal, formation of cell types and tissues. They also underlie environmental impacts on human health, including aging and diseases like cancer. Consequently, cracking the epigenetic "code" is considered a key challenge in biomedical research. Chromatin structure and function are modified by protein complexes, causing genes to be turned “on” or “off” and controlling other aspects of DNA function. Yet while there has been explosive growth in the epigenetics field, human chromatin-modifying machines have only recently started to be characterized. To meet this challenge, our book explores complementary experimental tracks, pursued by expert international research groups, aimed at the physical and functional characterization of the diverse repertoire of chromatin protein machines - namely, the "readers, writers and erasers" of epigenomic marks. These studies include the identification of RNA molecules and drugs that interact selectively with components of the chromatin machinery. What makes this book distinctive is its emphasis on the systematic exploration of chromatin protein complexes in the context of human development and disease networks.

This book includes a collection of articles with the broad theme of disease connection to chromatin structure and function. It elaborates on the molecular pharmacology of the drugs targeting chromatin structure and its components. The book contains up-to-date information about the chromatin structure and chromatin related diseases and drug functions. This work is the first endeavor to present different aspects encompassing the above theme.

There are now compelling human epidemiological and animal experimental data that indicate the risk of developing adult-onset complex diseases and neurological disorders are influenced by persistent epigenetic adaptations in response to prenatal and early postnatal exposures to environmental factors. Epigenetics refers to heritable changes in gene function that occur without a change in the sequence of the DNA. The main components of the epigenetic code are DNA methylation, histone modifications, and non-coding RNAs. The epigenetic programs are established as stem cell differentiate during embryogenesis, and they are normally faithfully reproduced during mitosis. Moreover, they can also be maintained during meiosis, resulting in epigenetic transgenerational disease inheritance, and also potentially introducing phenotypic variation that is selected for in the evolution of new species. The objective of this book is to provide evidence that environmental exposures during early development can alter the risk of developing medical conditions, such as asthma, autism, cancer, cardiovascular disease, diabetes, obesity, and schizophrenia later in life by modifying the epigenome.

​​​​​​​​​​​​​While there has been an increasing number of books on various aspects of epigenetics, there has been a gap over the years in books that provide a comprehensive understanding of the fundamentals of chromatin. ​Chromatin is the combination of DNA and proteins that make up the genetic material of chromosomes. Its primary function is to package DNA to fit into the cell, to strengthen the DNA to prevent damage, to allow mitosis and meiosis, and to control the expression of genes and DNA replication. The audience for this book is mainly newly established scientists ​and graduate students. Rather than going into the more specific areas of recent research on chromatin the chapters in this book give a strong, updated groundwork about the topic. Some the fundamentals that this book will cover include the structure of chromatin and biochemistry and the enzyme complexes that manage it.

Chromatin Signaling and Neurological Disorders, Volume Seven, explores our current understanding of how chromatin signaling regulates access to genetic information, and how their aberrant regulation can contribute to neurological disorders. Researchers, students and clinicians will not only gain a strong grounding on the relationship between chromatin signaling and neurological disorders, but they'll also discover approaches to better interpret and employ new diagnostic studies and epigenetic-based therapies. A diverse range of chapters from international experts speaks to the basis of chromatin and epigenetic signaling pathways and specific chromatin signaling factors that regulate a range of diseases. In addition to the basic science of chromatin signaling factors, each disease-specific chapter speaks to the translational or clinical significance of recent findings, along with important implications for the development of epigenetics-based therapeutics. Common themes of translational significance are also identified across disease types, as well as the future potential of chromatin signaling research. Examines specific chromatin signaling factors that regulate spinal muscular atrophy, ulbospinal muscular atrophy, amyotrophic lateral sclerosis, Parkinson's disease, Huntington's disease, multiple sclerosis, Angelman syndrome, Rader-Willi syndrome, and more Contains chapter contributions from international experts who speak to the clinical significance of recent findings and the implications for the development of epigenetics-based therapeutics Provides researchers, students and clinicians with approaches to better interpret and employ new diagnostic studies for treating neurological disorders