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Determining how defects in connexin43 cause skeletal disease
Author(s) -
Ton Quynh V.,
Iovine M. Kathryn
Publication year - 2013
Publication title -
genesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.093
H-Index - 110
eISSN - 1526-968X
pISSN - 1526-954X
DOI - 10.1002/dvg.22349
Subject(s) - gap junction , connexin , biology , microbiology and biotechnology , morphogenesis , function (biology) , intracellular , second messenger system , cell signaling , neuroscience , gene , signal transduction , genetics
Gap junction channels mediate direct cell–cell communication via the exchange of second messengers, ions, and metabolites from one cell to another. Mutations in several human connexin ( cx ) genes, the subunits of gap junction channels, disturb the development and function of multiple tissues/organs. In particular, appropriate function of Cx43 is required for skeletal development in all vertebrate model organisms. Importantly, it remains largely unclear how disruption of gap junctional intercellular communication causes developmental defects. Two groups have taken distinct approaches toward defining the tangible molecular changes occurring downstream of Cx43‐based gap junctional communication. Here, these strategies for determining how Cx43 modulates downstream events relevant to skeletal morphogenesis were reviewed. genesis 51:75–82, 2013. © 2012 Wiley Periodicals, Inc.