Document Detail


Determining how defects in Connexin43 cause skeletal disease.
MedLine Citation:
PMID:  23019186     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
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 towards 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 are reviewed. © 2012 Wiley Periodicals, Inc.
Authors:
Quynh V Ton; M Kathryn Iovine
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-9-28
Journal Detail:
Title:  Genesis (New York, N.Y. : 2000)     Volume:  -     ISSN:  1526-968X     ISO Abbreviation:  Genesis     Publication Date:  2012 Sep 
Date Detail:
Created Date:  2012-9-28     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100931242     Medline TA:  Genesis     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2012 Wiley Periodicals, Inc.
Affiliation:
Lehigh University, Department of Biological Sciences 111 Research Drive Iacocca B217.
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