Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2002-5-23
pubmed:abstractText
Gap junctions (Gj) play an important role in the communication between cells of many tissues. They are composed of channels that permit the passage of ions and low molecular weight metabolites between adjacent cells, without exposure to the extracellular environment. These pathways are formed by the interaction between two hemichannels on the surface of opposing cells. These hemichannels are formed by the association of six identical subunits, named connexins (Cx), which are integral membrane proteins. Cell coupling via Gj is dependent on the specific pattern of Cx gene expression. This pattern of gene expression is altered during several pathological conditions resulting in changes of cell coupling. The regulation of Cx gene expression is affected at different levels from transcription to post translational processes during injury. In addition, Gj cellular communication is regulated by gating mechanisms. The alteration of Gj communication during injury could be rationalized by two opposite theories. One hypothesis proposes that the alteration of Gj communication attenuates the spread of toxic metabolites from the injured area to healthy organ regions. The alternative proposition is that a reduction of cellular communication reduces the loss of important cellular metabolisms, such as ATP and glucose.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0021-9541
pubmed:author
pubmed:copyrightInfo
Copyright 2002 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:volume
191
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
269-82
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Gap junctions, homeostasis, and injury.
pubmed:affiliation
Division of Pediatric Surgery and Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. ademaio@mail.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't