Record Display for the EPA National Library Catalog

RECORD NUMBER: 230 OF 611

Main Title Gap Junctions in Development and Disease [electronic resource] /
Type EBOOK
Author Winterhager, Elke.
Publisher Springer Berlin Heidelberg,
Year Published 2005
Call Number QH573-671
ISBN 9783540286219
Subjects Life sciences ; Medicine ; Dermatology ; Otorhinolaryngology ; Reproductive Medicine ; Cytology ; Developmental biology
Internet Access
Description Access URL
http://dx.doi.org/10.1007/3-540-28621-7
Collation XVII, 279 p. 47 illus., 10 in color. online resource.
Notes
Due to license restrictions, this resource is available to EPA employees and authorized contractors only
Contents Notes
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. The main objective of Gap Junctions in Development and Disease is to describe the molecular events that cause impairments in development and disease. Communication between cells via intercellular channels, so called gap junctions, appears to be essential for certain developmental processes and appropriate organ function. Starting with a comprehensive review of the various mouse and human genes encoding the channel-forming protein connexin, further chapters describe the most important connexin mutations that lead to diseases such as hereditary deafness and female infertility in humans. Erroneous signaling mediated via connexin-protein interactions, thought to be responsible for disfunction of organs such as heart, muscle, brain, skin, lens, placenta, and endocrine tissue in mice and men, is also addressed. Although the question why some of the mutations in gap-junction proteins lead to a specific phenotype remains to be answered, the reviews in this book give an intriguing outlook on the future direction of this research field.