This indispensable volume highlights recent studies identifying epigenetic mechanisms as essential regulators of skin development, stem cell activity and regeneration. Chapters are contributed by leading experts and promote the skin as an accessible model system for studying mechanisms that control organ development and regeneration. The timely discussions contained throughout are of broad relevance to other areas of biology and medicine and can help inform the development of novel therapeutics for skin disorders as well as new approaches to skin regeneration that target the epigenome. Part of the highly successful Stem Cells and Regenerative Medicine series, Epigenetic Regulation of Skin Development and Regeneration uncovers the fundamental significance of epigenetic mechanisms in skin development and regeneration, and emphasizes the development of new therapies for a number of skin disorders, such as pathological conditions of epidermal differentiation, pigmentation and carcinogenesis. At least six categories of researchers will find this book essential, including stem cell, developmental, hair follicle or molecular biologists, and gerontologists or clinical dermatologists.

Autorentext

Vladimir Botchkarev, M.D., Ph.D., received his M.D. degree from Chuvash State University and his Ph.D. in Cell Biology from People Friendship University. He is Deputy Director of the Centre for Skin Sciences at the University of Bradford and Adjunct Professor of Dermatology at Boston University. Dr. Botchkarev's laboratory maintains a leading position in the research of signaling/transcription factor-mediated and epigenetic regulatory mechanisms that control stem cell activity, differentiation and reprogramming in the skin, as well as during skin regeneration and carcinogenesis. He has made seminal discoveries on the roles of BMP signaling pathway in the control of skin development and regeneration as well as on the roles of transcription factors in regulation of stem cell epigenome. Dr. Botchkarev serves on the Editorial Boards of many highly-respected journals in the field. During his career, he has received several awards and prizes in recognition of his research including an NIH Independent Scientist Award, Vice-Chancellor Outstanding Achievement Award and The Dermatology Foundation Research Career Development Award.

Sarah E. Millar, Ph.D., received her BA from Cambridge University and her Ph.D. from the University of London. Dr. Millar trained as a post-doctoral fellow at the NIH and at Stanford University. She was first appointed as a faculty member at the University of Pennsylvania and holds secondary appointments in the Department of Cell and Developmental Biology and in the School of Dental Medicine. She is Albert Kligman Professor and Vice-Chair for Basic Research in the Department of Dermatology at the University of Pennsylvania Perelman School of Medicine. Dr. Millar is P.I. and Director of the Penn Skin Biology and Diseases Resource-based Center, and P.I. of the Penn Dermatology Research training grant.

Inhalt

Preface.- Chapter 1 All Roads Go to the Nucleus.- Chapter 2 DNA methylation as an epigenetic memory keeper during skin development and regeneration.- Chapter 3 Polycomb genes and their roles in skin development and regeneration.- Chapter 4 Trithorax genes in the control of keratinocyte differentiation.- Chapter 5 Histone deacetylase functions in epidermal development, homeostasis and cancer.- Chapter 6 The role of ATP-dependent chromatin remodeling in the control of epidermal differentiation and skin stem cell activity.- Chapter 7 Orchestrated Role of microRNAs in Skin Development and Regeneration.- Chapter 8 Non-coding genome and its role in the control of gene expression.- Chapter 9 RNA modifications in the control of epidermal differentiation and stem cell activity.- Chapter 10 Enhancer-Promoter Interactions and Their Role in the Control of Epidermal Differentiation.- Chapter 11 Nuclear lamina as an interface between cytoskeleton and chromatin.- Chapter 12 Epigenetic mechanisms in the control of skin wound healing.