Linked Life Data

11125206

Source:http://linkedlifedata.com/resource/pubmed/id/11125206

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5-6
pubmed:dateCreated
2001-1-26
pubmed:abstractText
The following volume-sensitive channels are characterized in Ehrlich ascites tumor cells (EATC), (i) a tamoxifen- and AA acid sensitive, outwardly rectifying small anion channel (I(Cl,vol)) with low field anion selectivity (I(-)>Cl(-)) and moderate depolarisation-induced inactivation, (ii) a separate DIDS- and niflumic acid-sensitive organic osmolyte/anion channel (OOC) transporting predominantly taurine, and (iii) a clofilium- and Ba(2+)-sensitive, voltage- and Ca(2+)-insensitive 5 pS K(+) channel (I(K,vol)), resistant to a range of K(+) channel inhibitors including ChTX, clotrimazole, apamin, kaliotoxin, margatoxin, and TEA, and with a pH(o) dependence reminiscent of the two-pore domain background K(+) channels TASK. Cell swelling leads to an immediate and transient 3.3 fold increase in the rate of AA release resulting from activation of cPLA(2)alpha, which is found to be translocated to the nucleus upon cell swelling (probably to the inner nuclear membrane), where it is phosphorylated and activated by a G-protein coupled process. AA is a precursor for LTC(4), which is transported out of the cell, where it is converted to LTD(4), which activates I(K,vol), and OOC, whereas I(Cl,vol) is activated via a different pathway. In the absence of an increase in [Ca(2+)](i), the unitary conductance, kinetics, and pharmacological profile are similar for I(K,vol) and the K(+)-channels activated by LTD(4). Tyrosine phosphorylations are involved in the volume regulatory pathways and in defining the volume set-point. Tyrosin kinases appear to be involved in the signalling sequence leading to opening of the channels, and tyrosin phosphatases seem to be involved in closing of the channels. Finally a significant de-polymerization of F-actin is observed after cell swelling, the potential role of which in the volume regulatory mechanisms is under investigation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1015-8987
pubmed:author
pubmed:copyrightInfo
Copyright 2000 S. Karger AG, Basel.
pubmed:issnType
Print
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
273-88
pubmed:dateRevised
2009-11-3
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Intracellular signalling involved in volume regulatory decrease.
pubmed:affiliation
August Krogh Institute, Department of Biochemistry, University of Copenhagen, Copenhagen, Denmark. ekhoffmann@aki.ku.dk
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't