Linked Life Data

7835309

Source:http://linkedlifedata.com/resource/pubmed/id/7835309

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1995-3-2
pubmed:abstractText
TSH-induced intracellular Ca2+ concentration ([Ca2+]i) changes in single FRTL-5 thyroid cells were analyzed by digital video imaging of fura-2-loaded cells. More than 80% of the cells responded to as little as 30 nM TSH, resulting in a [Ca2+]i rise in the presence and absence of extracellular Ca2+. One micromolar concentration of N6-(L-2-phenylisopropyl)adenosine (PIA) caused no appreciable [Ca2+]i increase in more than 300 cells examined, but induced the [Ca2+]i elevation in more than 90% of the cells that had previously been treated with TSH. Pertussis toxin treatment abolished the PIA, but not the TSH, action, whereas thapsigargin-induced Ca2+ depletion of the inositol 1,4,5-trisphosphate-sensitive pool inhibited the actions of both TSH and PIA. The time courses of Ca2+ response considerably differentiated among single cells, but showed similarity among different areas in each cell. These results suggest that PIA induces Ca2+ release from the same thapsigargin-sensitive pool as that targeted by TSH. The lack of PIA stimulation of basic fibroblast growth factor-induced phospholipase-C gamma activation as well as the rise in [Ca2+]i suggests that the cooperative PIA action occurs specifically on phospholipase-C beta.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
136
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
770-8
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Cooperation of thyrotropin, but not basic fibroblast growth factor, with an adenosine receptor agonist in Ca2+ mobilization from thapsigargin-sensitive pools in single FRTL-5 thyroid cells.
pubmed:affiliation
Laboratory of Signal Transduction, Gunma University, Maebashi, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't