Linked Life Data

17166937

Source:http://linkedlifedata.com/resource/pubmed/id/17166937

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2007-5-14
pubmed:abstractText
The aquaporin (AQP)2 channel mediates the reabsorption of water in renal collecting ducts in response to arginine vasopressin (AVP) and hypertonicity. Here we show that AQP2 expression is induced not only by the tonicity-responsive enhancer binding protein (TonEBP)/nuclear factor of activated T cells (NFAT)5-mediated hypertonic stress response but also by the calcium-dependent calcineurin-NFATc pathway. The induction of AQP2 expression by the calcineurin-NFATc pathway can occur in the absence of TonEBP/NFAT5. Mutational and chromatin immunoprecipitation analyses revealed the existence of functional NFAT binding sites within the proximal AQP2 promoter responsible for regulation of AQP2 by NFATc proteins and TonEBP/NFAT5. Contrary to the notion that TonEBP/NFAT5 is the only Rel/NFAT family member regulated by tonicity, we found that hypertonicity promotes the nuclear translocation of NFATc proteins for the subsequent induction of AQP2 expression. Calcineurin activity was also found to be involved in the induction of TonEBP/NFAT5 expression by hypertonicity, thus further defining the signaling mechanisms that underlie the TonEBP/NFAT5 osmotic stress response pathway. The coordinate regulation of AQP2 expression by both osmotic stress and calcium signaling appears to provide a means to integrate diverse extracellular signals into optimal cellular responses.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0363-6143
pubmed:author
pubmed:issnType
Print
pubmed:volume
292
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
C1606-16
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:17166937-Active Transport, Cell Nucleus, pubmed-meshheading:17166937-Animals, pubmed-meshheading:17166937-Aquaporin 2, pubmed-meshheading:17166937-Calcineurin, pubmed-meshheading:17166937-Calcium Signaling, pubmed-meshheading:17166937-Cell Line, pubmed-meshheading:17166937-Epithelial Cells, pubmed-meshheading:17166937-Ionomycin, pubmed-meshheading:17166937-Ionophores, pubmed-meshheading:17166937-Kidney Tubules, Collecting, pubmed-meshheading:17166937-Mice, pubmed-meshheading:17166937-Mice, Knockout, pubmed-meshheading:17166937-Mutation, pubmed-meshheading:17166937-NFATC Transcription Factors, pubmed-meshheading:17166937-Osmosis, pubmed-meshheading:17166937-Promoter Regions, Genetic, pubmed-meshheading:17166937-Saline Solution, Hypertonic, pubmed-meshheading:17166937-Signal Transduction, pubmed-meshheading:17166937-Stress, Physiological, pubmed-meshheading:17166937-Tetradecanoylphorbol Acetate, pubmed-meshheading:17166937-Transcription, Genetic, pubmed-meshheading:17166937-Transcription Factors, pubmed-meshheading:17166937-Transfection, pubmed-meshheading:17166937-Up-Regulation, pubmed-meshheading:17166937-Water-Electrolyte Balance
pubmed:year
2007
pubmed:articleTitle
Calcineurin-NFATc signaling pathway regulates AQP2 expression in response to calcium signals and osmotic stress.
pubmed:affiliation
Department of Internal Medicine/Renal Division, Campus Box 8126, Washington University School of Medicine, St. Louis, MO 63110, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural