000 03489nam a22005295i 4500
001 978-3-540-28621-9
003 DE-He213
005 20161121230705.0
007 cr nn 008mamaa
008 100301s2005 gw | s |||| 0|eng d
020 _a9783540286219
_9978-3-540-28621-9
024 7 _a10.1007/3-540-28621-7
_2doi
050 4 _aQH573-671
072 7 _aPSF
_2bicssc
072 7 _aSCI049000
_2bisacsh
082 0 4 _a571.6
_223
245 1 0 _aGap Junctions in Development and Disease
_h[electronic resource] /
_cedited by Elke Winterhager.
264 1 _aBerlin, Heidelberg :
_bSpringer Berlin Heidelberg,
_c2005.
300 _aXVII, 279 p. 47 illus., 10 illus. in color.
_bonline resource.
336 _atext
_btxt
_2rdacontent
337 _acomputer
_bc
_2rdamedia
338 _aonline resource
_bcr
_2rdacarrier
347 _atext file
_bPDF
_2rda
505 0 _aConnexin 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.
520 _aThe 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.
650 0 _aLife sciences.
650 0 _aMolecular biology.
650 0 _aDermatology.
650 0 _aOtorhinolaryngology.
650 0 _aReproductive medicine.
650 0 _aCell biology.
650 0 _aDevelopmental biology.
650 1 4 _aLife Sciences.
650 2 4 _aCell Biology.
650 2 4 _aMolecular Medicine.
650 2 4 _aDevelopmental Biology.
650 2 4 _aOtorhinolaryngology.
650 2 4 _aReproductive Medicine.
650 2 4 _aDermatology.
700 1 _aWinterhager, Elke.
_eeditor.
710 2 _aSpringerLink (Online service)
773 0 _tSpringer eBooks
776 0 8 _iPrinted edition:
_z9783540261568
856 4 0 _uhttp://dx.doi.org/10.1007/3-540-28621-7
912 _aZDB-2-SBL
950 _aBiomedical and Life Sciences (Springer-11642)
999 _c502515
_d502515