Ulteriori informazioni
Communication between cells via intercellular channels - gap junctions - appears essential to certain developmental processes and appropriate organ function. Gap Junctions in Development and Disease aims to describe the molecular events underlying impaired development and disease. Beginning with a comprehensive review of various mouse and human genes encoding the channel-forming connexins, later chapters describe several connexin mutations associated with human diseases such as hereditary deafness and female infertility. Erroneous signaling mediated by the interaction of mutant connexins with other proteins, thought to be responsible for dysfunction of organs such as heart, muscle, brain, skin, lens, placenta, and endocrine tissue in both mice and men, is also addressed.
Although the question of why some mutations in gap-junction proteins lead to specific phenotypes remains to be answered, the reviews in this book provide an intriguing insight into the future direction of this research field.
Sommario
Connexin and Pannexin Genes in the Mouse and Human Genome.- Essential Role of Gap Junctions During Development and Regeneration of Skeletal Muscle.- Connexins in Cardiac Development: Expression, Role, and Transcriptional Control.- Gap Junction and Connexin Remodeling in Human Heart Disease.- Gap Junction Expression in Brain Tissues with Focus on Development.- Connexins Responsible for Hereditary Deafness - The Tale Unfolds.- Human Connexins in Skin Development and Skin Disorders.- Intercellular Communication in Lens Development and Disease.- Connexin Modulators of Endocrine Function.- Roles of Gap Junctions in Ovarian Folliculogenesis: Implications for Female Infertility.- Placental Connexins of Mice and Men.- Connexins in Growth Control and Cancer.
Riassunto
Communication between cells via intercellular channels – gap junctions – appears essential to certain developmental processes and appropriate organ function.
Gap Junctions in Development and Disease
aims to describe the molecular events underlying impaired development and disease. Beginning with a comprehensive review of various mouse and human genes encoding the channel-forming connexins, later chapters describe several connexin mutations associated with human diseases such as hereditary deafness and female infertility. Erroneous signaling mediated by the interaction of mutant connexins with other proteins, thought to be responsible for dysfunction of organs such as heart, muscle, brain, skin, lens, placenta, and endocrine tissue in both mice and men, is also addressed.
Although the question of why some mutations in gap-junction proteins lead to specific phenotypes remains to be answered, the reviews in this book provide an intriguing insight into the future direction of this research field.
