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Gap Junctions in Development and Disease [Hardcover]

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  • Category: Books (Science)
  • ISBN-10:  3540261567
  • ISBN-10:  3540261567
  • ISBN-13:  9783540261568
  • ISBN-13:  9783540261568
  • Publisher:  Springer
  • Publisher:  Springer
  • Pages:  279
  • Pages:  279
  • Binding:  Hardcover
  • Binding:  Hardcover
  • Pub Date:  01-Mar-2005
  • Pub Date:  01-Mar-2005
  • SKU:  3540261567-11-SPRI
  • SKU:  3540261567-11-SPRI
  • Item ID: 100785543
  • List Price: $169.99
  • Seller: ShopSpell
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  • Delivery by: Jul 04 to Jul 06
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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.

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 phelÓ)

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