Linked Life Data

1703278

Source:http://linkedlifedata.com/resource/pubmed/id/1703278

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
1991-2-26
pubmed:abstractText
In human T (Jurkat) lymphoblasts we have studied the calcium signals induced by monoclonal antibodies reacting with the T-cell antigen receptor complex (TCR and CD3). Jurkat cells were preloaded with the fluorescent calcium indicator Indo-1 and the stimulus-induced rise in cytoplasmic free calcium concn was followed in the absence or in the presence of external calcium. The technique allowed the separate investigation of the intracellular calcium release and the external calcium influx processes. The changes in the membrane potential of Jurkat cells were followed simultaneously by using fluorescent indicators. We found that the activation of protein kinase C by phorbol ester (PMA) or by the permeable diacyl glycerol, DiC8, rapidly eliminated the calcium signal, independently of the presence or absence of external calcium, while these treatments did not appreciably change the membrane potential. In contrast, cell membrane depolarization achieved by various treatments selectively blocked the stimulus-induced calcium influx, while did not affect stimulus-induced calcium release from internal stores. The magnitude of the stimulus-induced calcium influx was found to be largely independent of the external calcium concns between about 2-2500 microM. It is demonstrated that the inhibitory effect of membrane depolarization on calcium influx is not simply due to the reduction of the inward calcium gradient under these conditions. These observations indicate a significant down-regulation of the stimulus-induced calcium signal by protein kinase C activation and a selective inhibition of the receptor-operated calcium channels by membrane depolarization.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/1,2-dioctanoylglycerol, http://linkedlifedata.com/resource/pubmed/chemical/3,3'-dipropyl-2,2'-thiadicarbocyanin..., http://linkedlifedata.com/resource/pubmed/chemical/4-Chloromercuribenzenesulfonate, http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal, http://linkedlifedata.com/resource/pubmed/chemical/Benzothiazoles, http://linkedlifedata.com/resource/pubmed/chemical/Calcium, http://linkedlifedata.com/resource/pubmed/chemical/Carbocyanines, http://linkedlifedata.com/resource/pubmed/chemical/Diglycerides, http://linkedlifedata.com/resource/pubmed/chemical/Gramicidin, http://linkedlifedata.com/resource/pubmed/chemical/Muromonab-CD3, http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C, http://linkedlifedata.com/resource/pubmed/chemical/Tetradecanoylphorbol Acetate
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0161-5890
pubmed:author
pubmed:issnType
Print
pubmed:volume
27
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1297-306
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Regulation of stimulus-induced calcium transport pathways in human T (Jurkat) lymphoblasts.
pubmed:affiliation
National Institute of Haematology and Blood Transfusion, Budapest, Hungary.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't