Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1989-5-12
pubmed:abstractText
The mechanisms by which an activator of cyclic AMP-dependent protein kinase, corticotropin releasing factor (CRF) and the protein kinase C stimulant, phorbol myristate acetate (PMA) regulate the level of intracellular free calcium in the mouse anterior pituitary cell line AtT-20 were examined using the fluorescence probe Quin 2. The increase in cytosolic calcium in AtT-20 cells induced by CRF and PMA was blocked by calcium channel antagonists indicating that both agents stimulate calcium influx. The ability of PMA to raise cytosolic calcium levels was prevented by the sodium channel antagonist tetrodotoxin, suggesting that phorbol esters depolarize the cell membrane or increase action potential frequency to enhance calcium influx. The K+ channel antagonists, tetraethylammonium, cesium and 4-aminopyridine, inhibited PMA-stimulated calcium influx in AtT-20 cells. Thus, one mechanism by which protein kinase C activation may lead to a depolarization of the cell membrane is through a reduction in K+ currents. In contrast, neither tetraethylammonium or cesium reduced CRF-stimulated calcium influx into AtT-20 cells. The stimulation of calcium influx by CRF, therefore, appears to not involve changes in K+ currents in AtT-20 cells. CRF activates cyclic AMP-dependent protein kinase to stimulate calcium influx either by facilitating calcium conductance directly or by modifying the membrane potential or firing activity of AtT-20 cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0022-3565
pubmed:author
pubmed:issnType
Print
pubmed:volume
248
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
984-90
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
Phorbol esters and corticotropin releasing factor stimulate calcium influx in the anterior pituitary tumor cell line, AtT-20, through different intracellular sites of action.
pubmed:affiliation
Department of Pharmacology, University of Pennsylvania School of Medicine, Philadelphia.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't