rdf:type |
|
lifeskim:mentions |
umls-concept:C0001455,
umls-concept:C0004083,
umls-concept:C0020291,
umls-concept:C0031621,
umls-concept:C0031671,
umls-concept:C0031715,
umls-concept:C0033640,
umls-concept:C0034790,
umls-concept:C0086376,
umls-concept:C0108779,
umls-concept:C0178719,
umls-concept:C0205217,
umls-concept:C0205263,
umls-concept:C1948023
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pubmed:dateCreated |
1992-7-7
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pubmed:abstractText |
Modulation of inositol phospholipid (InsPL) hydrolysis in response to increasing intracellular concentrations of cyclic AMP (cAMP) was studied in a murine T helper type II (Th2) lymphocyte clone, 8-5-5. Intact 8-5-5 cells produced maximal amounts of cAMP in response to prostaglandin E2 (PGE2), cholera toxin (CTx) or 7 beta-deacetyl-7 beta-(gamma-N-methylpiperazino)butyryl forskolin (dmpb-forskolin). cAMP generation reached a plateau after 5 min of treatment with dmpb-forskolin (300 microM) or PGE2 (1 microM), but required 60 min of treatment with CTx (1 microgram/ml). Preincubation of 8-5-5 cells with 1 microM-PGE2 or 300 microM-dmpb-forskolin (10 min at 37 degrees C) or with 1 microgram of CTx/ml (60 min at 37 degrees C) completely inhibited InsPL hydrolysis induced by perturbation of the T cell receptor (TCR)/CD3 complex with the monoclonal antibody 145.2C11. Preincubation with the cAMP analogue 8-bromo-cyclic AMP (8-Br-cAMP) also inhibited InsPL hydrolysis. Tetanolysin-permeabilized 8-5-5 cells produced cAMP in response to PGE2, dmpb-forskolin and guanosine 5'-[gamma-thio]triphosphate (GTP[S]), a non-cell-permeating, non-hydrolysable analogue of GTP that directly activates G-proteins. No inhibition of TCR/CD3-induced InsPL hydrolysis was observed under these conditions. InsPL hydrolysis was also unaffected when permeabilized cells were incubated with up to 10 mM-8-Br-cAMP, suggesting that permeabilized cells lost (a) soluble effector molecule(s) involved in mediating the inhibitory effect observed in intact cells. Treatment of 8-5-5 cells with dmpb-forskolin or CTx prior to permeabilization resulted in inhibition of TCR/CD3-induced InsPL hydrolysis, but did not affect InsPL hydrolysis induced via G-protein stimulation with GTP[S]. Treatment of permeabilized 8-5-5 cells with purified cAMP-dependent protein kinase (PKA) resulted in inhibition of TCR/CD3- but not GTP[S]-induced InsPL hydrolysis. This effect was associated with phosphorylation of phospholipase (PLC)-gamma 1 in the absence of phosphorylation of components of the TCR/CD3 complex. These results suggest that PKA-mediated phosphorylation of PLC may regulate TCR/CD3-induced InsPL hydrolysis.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-1645519,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-1689750,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-1828897,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-1832154,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-2061301,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-210449,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-2137334,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-2138816,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-2162906,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-2164063,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-2165947,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-2211942,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-2443570,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-2459119,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-2472446,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-2479646,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-2555197,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-2562908,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-2648706,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-2764099,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-2824607,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-2828473,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-2829202,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-2839752,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-2855581,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-2875801,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-2939858,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-3016713,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-3021852,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-3028083,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-3038954,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-3104085,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-3104110,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-3141505,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-3155734,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-3600614,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-3918270,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-3919143,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-4375763,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-5432063,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-6146314,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-6194243,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1318020-6232463
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD3,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation...,
http://linkedlifedata.com/resource/pubmed/chemical/Cholera Toxin,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP,
http://linkedlifedata.com/resource/pubmed/chemical/Dinoprostone,
http://linkedlifedata.com/resource/pubmed/chemical/Forskolin,
http://linkedlifedata.com/resource/pubmed/chemical/GTP-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Inositol Phosphates,
http://linkedlifedata.com/resource/pubmed/chemical/Isoenzymes,
http://linkedlifedata.com/resource/pubmed/chemical/L 858051,
http://linkedlifedata.com/resource/pubmed/chemical/Phospholipids,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell,
http://linkedlifedata.com/resource/pubmed/chemical/Type C Phospholipases
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0264-6021
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
284 ( Pt 1)
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
189-99
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pubmed:dateRevised |
2010-9-7
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pubmed:meshHeading |
|