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.

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.

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.